Lovastatin: A fungal metabolite isolated from cultures of Aspergillus terreus. The compound is a potent anticholesteremic agent. It inhibits 3-hydroxy-3-methylglutaryl coenzyme A reductase (HYDROXYMETHYLGLUTARYL COA REDUCTASES), which is the rate-limiting enzyme in cholesterol biosynthesis. It also stimulates the production of low-density lipoprotein receptors in the liver.Hydroxymethylglutaryl-CoA Reductase Inhibitors: Compounds that inhibit HMG-CoA reductases. They have been shown to directly lower cholesterol synthesis.Mevalonic AcidAnticholesteremic Agents: Substances used to lower plasma CHOLESTEROL levels.Protein Prenylation: A post-translational modification of proteins by the attachment of an isoprenoid to the C-terminal cysteine residue. The isoprenoids used, farnesyl diphosphate or geranylgeranyl diphosphate, are derived from the same biochemical pathway that produces cholesterol.Polyisoprenyl Phosphates: Phosphoric or pyrophosphoric acid esters of polyisoprenoids.Hydroxymethylglutaryl CoA Reductases: Enzymes that catalyze the reversible reduction of alpha-carboxyl group of 3-hydroxy-3-methylglutaryl-coenzyme A to yield MEVALONIC ACID.Simvastatin: A derivative of LOVASTATIN and potent competitive inhibitor of 3-hydroxy-3-methylglutaryl coenzyme A reductase (HYDROXYMETHYLGLUTARYL COA REDUCTASES), which is the rate-limiting enzyme in cholesterol biosynthesis. It may also interfere with steroid hormone production. Due to the induction of hepatic LDL RECEPTORS, it increases breakdown of LDL CHOLESTEROL.Cholesterol: The principal sterol of all higher animals, distributed in body tissues, especially the brain and spinal cord, and in animal fats and oils.Drug Incompatibility: The quality of not being miscible with another given substance without a chemical change. One drug is not of suitable composition to be combined or mixed with another agent or substance. The incompatibility usually results in an undesirable reaction, including chemical alteration or destruction. (Dorland, 27th ed; Stedman, 25th ed)Pravastatin: An antilipemic fungal metabolite isolated from cultures of Nocardia autotrophica. It acts as a competitive inhibitor of HMG CoA reductase (HYDROXYMETHYLGLUTARYL COA REDUCTASES).Farnesol: A colorless liquid extracted from oils of plants such as citronella, neroli, cyclamen, and tuberose. It is an intermediate step in the biological synthesis of cholesterol from mevalonic acid in vertebrates. It has a delicate odor and is used in perfumery. (From McGraw-Hill Dictionary of Scientific and Technical Terms, 5th ed)Monascus: A genus in the family Monascaceae, order EUROTIALES. One species, Monascus purpureus, has multiple uses in traditional Chinese medicine (MEDICINE, CHINESE TRADITIONAL).Colestipol: Highly crosslinked and insoluble basic anion exchange resin used as anticholesteremic. It may also may reduce triglyceride levels.Aspergillus: A genus of mitosporic fungi containing about 100 species and eleven different teleomorphs in the family Trichocomaceae.Hydroxymethylglutaryl-CoA-Reductases, NADP-dependent: Specific hydroxymethylglutaryl CoA reductases that utilize the cofactor NAD. In liver enzymes of this class are involved in cholesterol biosynthesis.Fatty Acids, Monounsaturated: Fatty acids which are unsaturated in only one position.

Insulin and TSH promote growth in size of PC Cl3 rat thyroid cells, possibly via a pathway different from DNA synthesis: comparison with FRTL-5 cells. (1/983)

In the rat thyroid cell lines PC Cl3, FRTL- 5 and WRT, proliferation is mainly regulated by insulin or IGF, and TSH. However, the mechanism regulating cell mass doubling prior to division is still unknown. Our laboratory has shown that in dog thyroid cells insulin promotes growth in size while TSH in the presence of insulin triggers DNA replication. In the absence of insulin, TSH has no effect on cell growth. In this report we investigated insulin action on both cell mass and DNA synthesis and its modulation by TSH and insulin in PC Cl3 and FRTL-5 cells. In PC Cl3 cells, insulin activated not only DNA synthesis but also protein synthesis and accumulation. Although TSH potentiated the stimulation of DNA synthesis induced by insulin, enhancement of protein synthesis by both agents was additive. All TSH effects were reproduced by forskolin. Similar effects were also obtained in FRTL-5 cells. This suggests that insulin and TSH, via cAMP, modulate both growth in size and DNA replication in these cell lines. Lovastatin, which blocks 3-hydroxy-3-methylglutaryl coenzyme A reductase, decreased the induction of DNA synthesis, but not of protein synthesis induced by insulin or TSH in PC Cl3 cells. In FRTL-5 cells, lovastatin reduced protein and DNA synthesis stimulated by insulin but not TSH-induced protein synthesis. Taking these data together, we propose that insulin and/or TSH both modulate cell mass doubling and DNA synthesis in these cell lines, presumably via different pathways, and that there are at least two pathways which regulate growth in size in FRTL-5 thyroid cells: one triggered by insulin, which is lovastatin sensitive, and the other activated by TSH, which is not sensitive to lovastatin.  (+info)

Role of cholesterol ester mass in regulation of secretion of ApoB100 lipoprotein particles by hamster hepatocytes and effects of statins on that relationship. (2/983)

Our understanding of the factors that regulate the secretion of apoB100 lipoproteins remains incomplete with considerable debate as to the role, if any, for cholesterol ester in this process. This study examines this issue in primary cultures of hamster hepatocytes, a species in which both cholesterol and apoB100 metabolism are very similar to man. Addition of oleate to medium increased the mass of triglyceride and cholesterol ester within the hepatocyte and also increased the secretion of triglycerides, cholesterol ester, and apoB100 into the medium. Next, the responses of hamster hepatocytes to addition of either an HMG-CoA reductase inhibitor (lovastatin) or an acyl-CoA cholesterol acyltransferase inhibitor (58-035) to the medium, with or without added oleate, were determined. Effects of either agent were only evident in the oleate-supplemented medium in which cholesterol ester mass had been increased above basal. If oleate was not added to the medium, neither agent reduced apoB100 secretion; equally important, over the 24-hour incubation, neither agent, at the concentration used, produced any detectable change in intracellular cholesterol ester mass. However, in contrast to the estimates of mass, which were unchanged, under the same conditions radioisotopic estimates of cholesterol ester synthesis were markedly reduced. Any conclusion as to the relation of cholesterol ester mass to apoB100 secretion would therefore depend on which of the 2 methods was used. Overall, the data indicate a close correlation between the mass of cholesterol ester within the hepatocyte and apoB100 secretion from it and they go far to explain previous apparently contradictory data as to this relation. More importantly, though, taken with other available data, they indicate that the primary response of the liver to increased delivery of lipid is increased secretion rather than decreased uptake. These results point, therefore, to a hierarchy of hepatic responses to increased flux of fatty acids and increased synthesis of cholesterol that in turn suggests a more dynamic model of cholesterol homeostasis in the liver than has been appreciated in the past.  (+info)

Effect of inhibition of cholesterol synthetic pathway on the activation of Ras and MAP kinase in mesangial cells. (3/983)

Intermediary metabolites of cholesterol synthetic pathway are involved in cell proliferation. Lovastatin, an inhibitor of 3-hydroxy-3-methylglutaryl coenzyme A reductase, blocks mevalonate synthesis, and has been shown to inhibit mesangial cell proliferation associated with diverse glomerular diseases. Since inhibition of farnesylation and plasma membrane anchorage of the Ras proteins is one suggested mechanism by which lovastatin prevents cellular proliferation, we investigated the effect of lovastatin and key mevalonate metabolites on the activation of mitogen-activated protein kinase (MAP kinase) and Ras in murine glomerular mesangial cells. The preincubation of mesangial cells with lovastatin inhibited the activation of MAP kinase stimulated by either FBS, PDGF, or EGF. Mevalonic acid and farnesyl-pyrophosphate, but not cholesterol or LDL, significantly prevented lovastatin-induced inhibition of agonist-stimulated MAP kinase. Lovastatin inhibited agonist-induced activation of Ras, and mevalonic acid and farnesylpyrophosphate antagonized this effect. Parallel to the MAP kinase and Ras data, lovastatin suppressed cell growth stimulated by serum, and mevalonic acid and farnesylpyrophosphate prevented lovastatin-mediated inhibition of cellular growth. These results suggest that lovastatin, by inhibiting the synthesis of farnesol, a key isoprenoid metabolite of mevalonate, modulates Ras-mediated cell signaling events associated with mesangial cell proliferation.  (+info)

Posttranslational regulation of the retinoblastoma gene family member p107 by calpain protease. (4/983)

The retinoblastoma protein plays a critical role in regulating the G1/S transition. Less is known about the function and regulation of the homologous pocket protein p107. Here we present evidence for the posttranslational regulation of p107 by the Ca2+-activated protease calpain. Three negative growth regulators, the HMG-CoA reductase inhibitor lovastatin, the antimetabolite 5-fluorouracil, and the cyclic nucleotide dibutyryl cAMP were found to induce cell type-specific loss of p107 protein which was reversible by the calpain inhibitor leucyl-leucyl-norleucinal but not by the serine protease inhibitor phenylmethylsulfonylfluoride, caspase inhibitors, or lactacystin, a specific inhibitor of the 26S proteasome. Purified calpain induced Ca2+-dependent p107 degradation in cell lysates. Transient expression of the specific calpain inhibitor calpastatin blocked the loss of p107 protein in lovastatin-treated cells, and the half-life of p107 was markedly lengthened in lovastatian-treated cells stably transfected with a calpastatin expression vector versus cells transfected with vector alone. The data presented here demonstrate down-regulation of p107 protein in response to various antiproliferative signals, and implicate calpain in p107 posttranslational regulation.  (+info)

Effects of LY295427, a low-density lipoprotein (LDL) receptor up-regulator, on LDL receptor gene transcription and cholesterol metabolism in normal and hypercholesterolemic hamsters. (5/983)

The action of LY295427 [(3alpha,4alpha, 5alpha)-4-(2-propenylcholestan-3-ol)], a compound that derepresses low-density lipoprotein receptor (LDL-R) expression in a cell-based model, was examined in hamsters. It was found that the compound does not have an effect in normal chow-fed hamsters, in which LDL-R levels are not repressed, but exerts a marked hypocholesterolemic effect (>70% decrease) in cholesterol-coconut oil-fed hamsters, in which LDL-R is repressed. In this model, there is a dose-response for cholesterol lowering with an approximate ED50 value of 40 mg/kg/day and an inverse relationship between serum cholesterol and serum LY295427 levels. LDL-R mRNA is increased (2-fold) and liver cholesterol ester content is decreased (>90%). Unlike the 3-hydroxy-3-methylglutarylcoenzyme A reductase inhibitor lovastatin, the decreased serum cholesterol is confined to the non-high-density lipoprotein fraction. Furthermore, LY295427 does not affect cholesterol biosynthesis, and it does not have a significant effect on cholesterol absorption. These data suggest that LY295427 acts in the hypercholesterolemic hamster by derepressing LDL-R transcription, thereby enhancing cholesterol clearance from the blood. The results with LY295427 suggest that compounds that act to increase LDL-R may represent a novel approach in the pharmacotherapy for hypercholesterolemia.  (+info)

Lovastatin-induced proliferation inhibition and apoptosis in C6 glial cells. (6/983)

3-Hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase is the rate-limiting enzyme in cholesterol biosynthesis. HMG-CoA reductase converts HMG-CoA to mevalonate, which is then converted into cholesterol or various isoprenoids through multiple enzymatic steps. In this study, we examined the cytotoxic effects of lovastatin, an HMG-CoA reductase inhibitor, in C6 glial cells. Lovastatin at concentrations higher than 10 microM suppressed cell proliferation and induced cell death, which were prevented completely by mevalonate (300 microM). The data from lactate dehydrogenase assay and fluorescence microscopic assay using Hoechst 33342 and propidium iodide showed that mevalonate at a concentration of 100 microM could prevent lovastatin-induced cell death, whereas it could not prevent lovastatin-induced inhibition of cell proliferation. These data suggest that the lovastatin-induced interruption of cell cycle transition was not sufficient to induce cell death in C6 glial cells. In the presence of lovastatin at concentrations higher than 10 microM, DNA laddering, the typical finding of apoptosis, was identified. Lovastatin-induced apoptosis was prevented by mevalonate (100 microM). Both cycloheximide (0.5 microgram/ml) and actinomycin D (0.1 microgram/ml) prevented lovastatin-induced DNA laddering. In this study, we demonstrated that the cytotoxic effects of lovastatin fall into two categories: suppression of cell growth and induction of apoptosis in C6 glial cells.  (+info)

Postmarketing analysis of lovastatin use in the VA Northern California System of Clinics: a retrospective, computer-based study. (7/983)

Prevention of coronary heart disease is a major public health goal. The efficacy of lovastatin in lowering serum cholesterol has been proven in research studies, but its efficacy in practice is unclear. To evaluate our practice patterns and outcome in the Veterans Administration Northern California System of Clinics, we reviewed computer-based records of 203 unselected patients issued lovastatin; 193 (95%) were men, and the average patient age was 66 +/- 9 years. The average daily dose of lovastatin was 24 +/- 10 mg, and average duration of therapy was 22 +/- 11 months. Only 72 patients (35%) were instructed on the prescription to take their medication with the evening meal, and only 59 patients (29%) had seen a dietitian during the observed (1 to 3 years) treatment period. Nevertheless, among the 124 patients with pretreatment lipid data, total serum cholesterol decreased by 18% from 271 +/- 45 to 221 +/- 41 mg/dL (P < 0.001), and low density lipoprotein (LDL)-cholesterol decreased by 23% from 185 +/- 43 to 143 +/- 37 (P < 0.001) mg/dL. High density lipoprotein-cholesterol and triglycerides were unchanged. Of the 168 patients with LDL-cholesterol data during the treatment period, only 74 (44%) achieved an LDL-cholesterol level of less than 130 mg/dL, the minimum goal for a population of older males with a high incidence of other cardiac risk factors. Safety surveillance with liver function testing was performed at least once in 192 patients (95%), but with creatine phosphokinase (CPK) testing in only 123 patients (61%) during the survey period. Enzyme elevations were minor, but occurred at least intermittently in approximately one quarter of patients. Only 5.7% of patients on lovastatin manifested an increase in transaminases on therapy. Due to incomplete baseline data, it is unclear how many patients had elevated CPK as a result of lovastatin. We conclude that: (1) lovastatin is effective in lowering total and LDL-cholesterol in practice, but is often used in dosage insufficient to lower LDL-cholesterol to goal levels; (2) patients are not being adequately educated on dosing schedules; (3) toxicity may be underestimated by infrequent and inconsistent surveillance; and (4) nonpharmacologic therapy is underutilized.  (+info)

The prenylation status of a novel plant calmodulin directs plasma membrane or nuclear localization of the protein. (8/983)

Post-translational attachment of isoprenyl groups to conserved cysteine residues at the C-terminus of a number of regulatory proteins is important for their function and subcellular localization. We have identified a novel calmodulin, CaM53, with an extended C-terminal basic domain and a CTIL CaaX-box motif which are required for efficient prenylation of the protein in vitro and in vivo. Ectopic expression of wild-type CaM53 or a non-prenylated mutant protein in plants causes distinct morphological changes. Prenylated CaM53 associates with the plasma membrane, but the non-prenylated mutant protein localizes to the nucleus, indicating a dual role for the C-terminal domain. The subcellular localization of CaM53 can be altered by a block in isoprenoid biosynthesis or sugar depletion, suggesting that CaM53 activates different targets in response to metabolic changes. Thus, prenylation of CaM53 appears to be a novel mechanism by which plant cells can coordinate Ca2+ signaling with changes in metabolic activities.  (+info)

*Lovastatin

"Lovastatin". MedlinePlus. U.S. National Library of Medicine. 15 June 2012. Retrieved 1 December 2012. "Lovastatin". LactMed. U. ... This led to the discovery of a novel fungal metabolite - lovastatin. The structure of lovastatin was determined to be different ... "Lovastatin". The American Society of Health-System Pharmacists. Retrieved 3 April 2011. "Mevacor, Altoprev (lovastatin) dosing ... Key points from the study of the biosynthesis of lovastatin: Lovastatin is composed of two polyketide chains derived from ...

*Niacin/lovastatin

... (trade names Advicor, Mevacor) is a drug combination used for the treatment of dyslipidemia. It is a ... combination of the vitamin niacin and the statin drug lovastatin. The combination preparation is marketed by Abbott ...

*Lovastatin nonaketide synthase

In enzymology, lovastatin nonaketide synthase (EC 2.3.1.161) is an enzyme that catalyzes the chemical reaction acetyl-CoA + 8 ... "Lovastatin nonaketide synthase catalyses an intramolecular Diels-Alder reaction of a substrate analogue". J. Am. Chem. Soc. 122 ...

*DMOZ - Health: Pharmacy: Drugs and Medications: L: Lovastatin

Lovastatin is a cholesterol-reducing drug.

*Pleurotus ostreatus

Oyster mushrooms produce the cholesterol lowering drug lovastatin.[citation needed] List of Pleurotus species Kummer, P. (1871 ...

*ConsumerLab.com

The study finds that 12 samples sent for testing had a per-capsule lovastatin level of: mean 2.54 mg, median 2.12 mg with a ... Red yeast rice contains a compound called lovastatin. ...

*Steroidogenesis inhibitor

Examples of statins include atorvastatin, lovastatin, rosuvastatin, and simvastatin. They are used in the treatment of ...

*Simvastatin

Tobert JA (2003). "Lovastatin and beyond: the history of the HMG-CoA reductase inhibitors". Nat Rev Drug Discov. 2 (7): 517-26 ... The development of simvastatin was closely linked with lovastatin. Biochemist Jesse Huff and his colleagues at Merck began ... In 1979, Hoffman and colleagues isolated lovastatin from a strain of the fungus Aspergillus terreus. While developing and ... researching lovastatin, Merck scientists synthetically derived a more potent HMG-CoA reductase inhibitor from a fermentation ...

*Atherosclerosis

May 1998). "Primary prevention of acute coronary events with lovastatin in men and women with average cholesterol levels: ... 1991). "Expanded Clinical Evaluation of Lovastatin (EXCEL) study results. I. Efficacy in modifying plasma lipoproteins and ...

*Clarithromycin

Concomitant use with cholesterol medications such as lovastatin or simvastatin. Hypersensitivity to clarithromycin or any ...

*CENPF

Holstein SA, Hohl RJ (2003). "Synergistic interaction of lovastatin and paclitaxel in human cancer cells". Mol. Cancer Ther. 1 ...

*Aspergillus terreus

Lovastatin is typically produced within fermentation conditions of the fungus. Fast growth of filamentous hyphae in the species ... It was also the initial source for the drug mevinolin (lovastatin), a drug for lowering serum cholesterol. A. terreus can cause ... Lopez, J.L; Perez J.L.; Sevilla J.M.; Fernandez FG.; Grima E.; Chisti Y (2003). "Production of lovastatin by Aspergillus ... doi:10.1016/s0141-0229(03)00130-3. Szakacs, G; Morovjan G.; Tengerdy R (1998). "Production of lovastatin by a wild strain of ...

*Medicinal fungi

Lovastatin, the first commercial statin, was extracted from a fermentation broth of Aspergillus terreus. Industrial production ... Jahromi, M.F.; Liang, J.B.; Ho, Y.W.; Mohamad R.; Goh, Y.M.; Shokryazdan, P. (2012). "Lovastatin production by Aspergillus ... Tolbert, Jonathan A. (2003). "Lovastatin and beyond: the history of the HMG-CoA reductase inhibitors". Nature Reviews Drug ... Other compounds include Simvastatin, a semi-synthetic derivative of Lovastatin. Some antifungals are derived or extracted from ...

*Pharmaceutical industry

By 1978, Merck had isolated lovastatin (mevinolin, MK803) from the fungus Aspergillus terreus, first marketed in 1987 as ... ". "Brochure: The History of Drug Regulation in the United States". Tobert, Jonathan A. (July 2003). "Lovastatin and beyond: ...

*Fungi in human culture

Jahromi, M.F.; Liang, J.B.; Ho, Y.W.; Mohamad, R.; Goh, Y.M., Shokryazdan, P. (2012). "Lovastatin production by Aspergillus ... The first commercial statin, lovastatin, was fermented by the mould Aspergillus terreus. Numerous anti-cancer drugs such as the ... Tolbert, Jonathan A. (2003). "Lovastatin and beyond: the history of the HMG-CoA reductase inhibitors". Nature Reviews Drug ...

*Discovery and development of statins

Simvastatin and lovastatin are inactive lactones which must be metabolized to their active hydroxy-acid forms in order to ... Lovastatin and simvastatin are administered in their lactone forms, which is more lipophilic than their free acid forms, and ... Tobert, Jonathan A. (July 2003). "Lovastatin and beyond: The history of the HMG-CoA reductase inhibitors". Nature Reviews Drug ... Statins that belong to this group are: Lovastatin (Figure 2) Pravastatin Simvastatin Type 2 statins Statins that are fully ...

*Coxsackie virus and adenovirus receptor

Werner B, Dittmann S, Funke C, Überla K, Piper C, Niehaus K, Horstkotte D, Farr M (Apr 2014). "Effect of lovastatin on ...

*Mevastatin

The first statin drug available to the general public was lovastatin. Mevastatin has since been derivatized to the compound ... lovastatin and mevastatin inhibit proliferation and invasion of melanoma cells". BMC Cancer. 8: 9. doi:10.1186/1471-2407-8-9. ...

*Red yeast rice

If they do not contain lovastatin, do not claim to contain lovastatin, and do not make a claim to lower cholesterol, they are ... Lovastatin became the patented, prescription drug Mevacor for Merck & Co. Red yeast rice went on to become a contentious non- ... Lovastatin and other prescription "statin" drugs inhibit cholesterol synthesis by blocking action of the enzyme HMG-CoA ... The Food and Drug Administration (FDA) position is that red yeast rice products that contain monacolin K, i.e., lovastatin, are ...

*1987 in science

August 31 - The FDA for the first time approves a statin, lovastatin. September 5 - The first successful surgical separation of ...

*Fungal isolate

The statins lovastatin, mevastatin, and simvastatin precursor monacolin J, are fungal isolates. Additional fungal isolates that ...

*Industrial fermentation

Some examples of secondary metabolites are penicillin, cyclosporin A, gibberellin, and lovastatin. Primary metabolites are ...

*Alcino J. Silva

Acosta, MT; Kardel, PG; Walsh, KS; Rosenbaum, KN; Gioia, GA; Packer, RJ (Oct 2011). "Lovastatin as treatment for neurocognitive ... Sebti, SM; Tkalcevic, GT; Jani, JP (1991). "Lovastatin, a cholesterol biosynthesis inhibitor, inhibits the growth of human H- ... They discovered that Lovastatin, a statin that crosses the blood-brain barrier, at a dose that does not affect control mice, ... "Lovastatin regulates brain spontaneous low-frequency brain activity in neurofibromatosis type 1". Neurosci. Lett. 515 (1): 28- ...

*Themis Medicare

Products include simvastatin, lovastatin, propofol, ethambutol, dimethyl isosorbide, artesunate, lumefenterine and arteether. ...

*Merck & Co.

Merck scientists also developed lovastatin, the first drug of the statin class. It was marketed under the trade name Mevacor. ...
We have shown that inhibition of HMG CoA reductase in vascular endothelial cells upregulates the expression and activity of ecNOS and prevents their downregulation by ox-LDL. The inhibitory effects of simvastatin or lovastatin on endothelial HMG CoA reductase were concentration-dependent and specific since their effects on ecNOS corresponded to their respective IC50s and could be bypassed and reversed with l-mevalonate.27 The mechanisms by which HMG CoA reductase inhibitors increase ecNOS expression occurs through an increase in ecNOS mRNA stability. Our findings, therefore, provide important counterregulatory mechanisms by which HMG CoA reductase inhibitors can preserve ecNOS expression in the presence of ox-LDL. This novel effect of HMG CoA reductase inhibitors on ecNOS expression could contribute to the restoration of endothelial function beyond that achieved by reduction in serum cholesterol levels.. Although hyperoxic conditions (ie, 95% O2) increase ecNOS gene transcription as we have ...
This hypothesis of a block in delivery of intracellular cholesterol to the cell membrane is compatible with the results of our radioisotope experiments. Other steps in cholesterol transport within the cells appear not to have been perturbed by lovastatin. The binding of AcLDL to the scavenger receptor in our cells was normal, as previously described in this and other systems.14 32 Uptake of radiolabeled cholesterol via AcLDL appeared to be normal under treatment with lovastatin (Table 1⇑ and Figure 3⇑), in contrast to results obtained by Bernini et al32 in murine macrophages. Our data (Figure 3⇑) and those of Kempen et al14 indicate that ACAT is not inhibited by statins. Yet the amount of cholesteryl oleate formed within the cells was reduced on lovastatin treatment (Figure 3⇑), consistent with a reduced delivery of substrate. Might there also be a problem with delivery of the fatty acid moiety for cholesteryl ester formation? Our data indicate that this is not the case. In cells ...
General Lovastatin may elevate creatine phosphokinase and transaminase levels (see WARNINGS and ADVERSE REACTIONS). This should be considered in the differential diagnosis of chest pain in a patient on therapy with lovastatin. Homozygous Familial Hypercholesterolemia Lovastatin is less effective in patients with the rare homozygous familial hypercholesterolemia, possibly because these patients have no functional LDL receptors. Lovastatin appears to be more likely to raise serum transaminases (see ADVERSE REACTIONS) in these homozygous patients. Information for Patients Patients should be advised about substances they should not take concomitantly with lovastatin and be advised to report promptly unexplained muscle pain, tenderness, or weakness particularly if accompanied by malaise or fever or if muscle signs and symptoms persist after discontinuing lovastatin (see list below and WARNINGS, Myopathy/Rhabdomyolysis). Patients should also be advised to inform other physicians prescribing a new ...
Study Design. This is a prospective multi-centre randomized, placebo-controlled Phase II study to determine the efficacy of Lovastatin ™ on visual spatial learning and/or attention abilities of children with NF1 aged between 8 and less than 16 years. In addition, the effect of Lovastatin ™ on secondary measures of executive function, visual spatial skills, behavior and quality of life will be assessed. Participants will be randomized to 16-weeks of treatment with Lovastatin ™ or a matched placebo. It is plausible and ethical to employ a placebo group as no standard therapy with established efficacy is being withheld. There is no cross-over in this study due to a lack of data concerning the length of possible washout effects. The Lovastatin ™ dose will begin at 20 mg once daily/continuous dosing and escalate over a two-week period to 40 mg once daily/continuous dosing and continue at this dose for 14 weeks. Participants will be carefully monitored for side effects. The safety of ...
Interstitial fibrosis is recognised as the best histological predictor of progressive renal disease. Myofibroblasts contribute to this process through several functions including hyperproliferation, collagen and collagenase synthesis and reorganisation of extracellular matrix. Recent limited in vitro studies suggest that 3-hydroxy-3-methylglutaryl-coenzyme A (HIVIG CoA) reductase inhibitors may reduce renal injury not only through their lipid-lowering effects but also by antagonising myofibroblast function. This study therefore examined the effects of lovastatin on the above interstitial myofibroblast behaviours in vitro. Primary cultures of rat renal cortical myofibroblasts were grown by explantation and characterised by immunohistochemistry. Dose response effects of lovastatin (0, 15,30 muM) in DMEM and 10% FCS were examined on myofibroblast kinetics, total collagen synthesis, collagen I lattice contraction and actin filament rearrangement. Lovastatin decreased myofibroblast proliferation and ...
Talks should maintain a closed index of suspicion for serious is lovastatin generic reactions to minocycline including lymphocytic violence and cerebral edema among HIV-positive maestros, especially if they are of Typhoid origin. Teer alternatives should be considered for treatment of abstinence vulgaris. Nephritis: Minocycline has been studied to cause serious, as rare, is lovastatin generic events, including serum saliva-like reaction, hypersensitivity syndrome reaction, and drug-induced audience. A is lovastatin generic review of people seen in our Adverse Piece Reaction Clinic as well as information tackled from the Health. Minocycline has been available to cause rare life-threatening events, such as rhinitis syndrome reaction, serum sicknesslike reaction and download-induced lupus erythematosus. A scalp of the Amount Safety Clinic database (from through ), the Constipation Protection Branch intermediate (from 7Roca, B. Calvo, B. Mevacor (lovastatin) is a cholesterol-lowering medication ...
Both retinoids and anti-estrogens inhibit breast cancer cell proliferation with accumulation of cells in the G1 phase of the cell cycle, but the effect of retinoids is delayed compared to that of anti-estrogens. To determine whether this temporal difference is due to a simple delay in the action of retinoids on a common site or to different sites of action within the G1 phase, we studied the cell cycle effects of retinoic acid (RA) and the anti-estrogen ICI 164384 (ICI) in T-47D cells partially synchronized by mevalonic acid rescue of lovastatin-induced cell cycle arrest. We found that cells entering the cell cycle semi-synchronously after mevalonic acid rescue of lovastatin treatment were immediately susceptible to ICI but not RA. This suggests that RA may act at a point up-stream and ICI at a point down-stream of lovastatin action. Consistent with this, cells recommencing cell cycle progression after RA treatment were susceptible to the effects of lovastatin, while cells pre-treated with ICI then
Lovastatin - Get up-to-date information on Lovastatin side effects, uses, dosage, overdose, pregnancy, alcohol and more. Learn more about Lovastatin
Simvastatin and lovastatin are statins traditionally used for lowering serum cholesterol levels. However, there exists evidence indicating their potential chemotherapeutic characteristics in cancer. In this study, we used bioinformatic analysis of publicly available data in order to systematically identify the genes involved in resistance to cytotoxic effects of these two drugs in the NCI60 cell line panel. We used the pharmacological data available for all the NCI60 cell lines to classify simvastatin or lovastatin resistant and sensitive cell lines, respectively. Next, we performed whole-genome single marker case-control association tests for the lovastatin and simvastatin resistant and sensitive cells using their publicly available Affymetrix 125K SNP genomic data. The results were then evaluated using RNAi methodology. After correction of the p-values for multiple testing using False Discovery Rate, our results identified three genes (NRP1, COL13A1, MRPS31) and six genes (EAF2, ANK2, AKAP7, STEAP2,
Mevacor is an efficient medication that is used to treat high triglycerides and high cholesterol. The generic name of this medicine is Lovastatin. Lovastatin is related to the set of drugs called cholesterol-lowering medications.
... As this eMedTV article explains, lovastatin is a drug that is used for the treatment of high cholesterol, as well as the prevention of heart disease. This page also discusses lovastatin use in children.
the affected area can no longer move leading to permanent disability by the sufferer. Read the labels of all the foods you purchase to make sure of what you are getting. where can i buy lovastatin 20 mg can i buy lovastatin the chemist then make sure you do your share of the homework and find out the most practical hair loss solutions to help you ...
Lists the various brand names available for medicines containing lovastatin. Find information on lovastatin use, treatment, drug class and molecular formula.
The heterotrimeric G protein G0 is highly enriched in the growth cones of neuronal cells and makes up 10% of the membrane protein of growth cones from neonatal rat brain. We have used PC12 cells, a cell line that differentiates to a neuron-like phenotype, as a model with which to study the mechanism of G protein localization. First, the role of the beta gamma-subunit was investigated. The attachment of the beta gamma-subunit to the membrane depends on the isoprenylation of the gamma-subunit. The drug lovastatin blocks isoprenylation by inhibiting a key enzyme in the biosynthetic pathway. After treatment of PC12 cells with 10 microM lovastatin for 48 hours 50% of the beta gamma-subunits were cytosolic compared with 100% membrane bound beta gamma in control cells, as determined by cell fractionation, gel electrophoresis and western blot. Addition of 200 microM mevalonic acid reverses this effect. However, lovastatin affects neither the membrane attachment of alpha 0 nor its localization to the ...
Some of the drugs that can interact with lovastatin include danazol, niacin, and fibrates. As this eMedTV page explains, some of the drug interactions with lovastatin can cause severe side effects and complications, including serious muscle problems.
1 Answer (question resolved) - Posted in: lovastatin - Answer: It doesnt appear to be a known side effect of lovastatin ... but may be ...
Sigma-Aldrich offers abstracts and full-text articles by [Manal Elfakhani, Sheida Torabi, Deema Hussein, Nathaniel Mills, Guido F Verbeck, Huanbiao Mo].
Clinical trials with compactin had been proceeding, but for reasons that have never been made public (but which were believed to include serious animal toxicity) the trials were stopped by Sankyo in September 1980. Because of the close structural similarity between compactin and lovastatin,cheap jerseys Merck promptly suspended clinical studies with lovastatin, and initiated additional animal safety studies. The future of the drug seemed extremely doubtful. Everyone of us here is like. His job the most unbelievable story you want to take a closer look at this work. Fifty others landscapes are currently on exhibit at Manhattans Fuller building you can buy one for a lot a lot of money are so beautiful beautiful Craig should right.. If it has reinforcement in the back make sure to cut below that. Keep the neckband intact as a ring. Stretch the neckband (not the shirt) to fit the new opening, and pin in place with right edges together. Olympic qualifying team alongside the likes of Tim Duncan and ...
LOVASTATIN (LOE va sta tin) is known as a HMG-CoA reductase inhibitor or statin. It lowers the level of cholesterol in the blood. This drug may also reduce the risk of heart attack or other health problems in patients with risk factors for heart disease. Diet and lifestyle changes are often used with this drug.
LOVASTATIN (LOE va sta tin) is known as a HMG-CoA reductase inhibitor or statin. It lowers the level of cholesterol in the blood. This drug may also reduce the risk of heart attack or other health problems in patients with risk factors for heart disease. Diet and lifestyle changes are often used with this drug.
Recognition of the abilities of FTIs or statins to induce autophagy is a recent development. Exposure of U2OS cultures to micromolar concentrations of lonafarnib or manumycin A, two FTIs with different modes of action, induces autophagy (Pan et al., 2008) as do the statins fluvastatin and simvastatin in some (Araki and Motojima, 2008), but not all (Martinet et al., 2008), types of cultured cells. In the case of the statin study, it was concluded that the induction of autophagy reflected an inhibition of prenylation because the effects of statin treatment could be blocked by the addition of mevalonate but not cholesterol. In the current study, exposure of MPNST STS-26T cells to nanomolar concentrations of FTI-1 plus lovastatin, but not to either agent alone, induced cell cycle arrest, a dysfunctional autophagic program, and nonapoptotic death. The induction of these processes by combined but not single treatments with FTI-1 or lovastatin occurred with concentrations of agents sufficient to ...
Lovastatin is a prescription medication used to reduce cholesterol levels, used along with a restricted diet to lower total cholesterol and LDL...
Potential lovastatin side effects may be exacerbated by interactions with other prescription drugs and medications or over-the-counter products.
Learn about Mevacor (Lovastatin) may treat, uses, dosage, side effects, drug interactions, warnings, patient labeling, reviews, and related medications.
Stock Photo 4128R-18517: Download Lovastatin, molecular model. Drug used for treating dyslipidemia and for prevention of cardiovascular disease. Atoms are represented as spheres and are colour_coded: carbon grey, hydrogen white and oxygen red. Stock Photos. Search over 12 million royalty free images and rights managed stock photography
Take this medication exactly as it was prescribed for you. Do not take the medication in larger amounts, or take it for longer than recommended by your doctor. Follow the directions on your prescription label.. Take lovastatin with a full glass of water. Do not crush, chew, or break an extended-release tablet. Swallow the pill whole. It is specially made to release medicine slowly in the body. Breaking or opening the pill would cause too much of the drug to be released at one time. Lovastatin is usually taken at bedtime or with an evening meal. If you take lovastatin several times daily, take it with meals. Follow your doctors instructions.. To be sure this medication is helping your condition, your blood will need to be tested on a regular basis. Your liver function may also need to be tested. Do not miss any scheduled appointments.. In rare cases, lovastatin can cause a condition that results in the breakdown of skeletal muscle tissue. This condition can lead to kidney failure. Call your ...
Before you begin using a medication, be sure to inform your doctor of any medical conditions or allergies you may have, any medications you are taking, whether you are pregnant or breast-feeding, and any other significant facts about your health. These factors may affect how you should use this medication.. Alcohol: The combination of alcohol use while taking lovastatin can increase the risk of harm to the liver. People who drink large quantities of alcohol should be closely monitored by their doctor while they are taking this medication.. Diabetes: Lovastatin may cause an increase in blood sugar levels (may cause a loss of blood glucose control) and glucose tolerance may change.People with diabetes may find it necessary to monitor their blood sugar more frequently while using this medication.. If you have diabetes or are at risk for developing diabetes, discuss with your doctor how this medication may affect your medical condition, how your medical condition may affect the dosing and ...
My research is mainly focused on the effects of cholesterol, saturated fat and statin drugs on health. If you know anyone who is worried about their cholesterol levels and heart disease, or has been told to take statin drugs you could send them a link to this website, and to my statin or cholesterol or heart disease books ...
Here i-Fect is used to silence miR-21 microRNAs. This miRNA stimulates pro-inflammatory pathways that are at the root of Coronary Heart Disease: Guo Weizao, Liu Huichen, Li Lin, Yang Man and Du Aihua. Regulation of lovastatin on a key inflammation-related microRNA in myocardial cells. Chinese Medical Journal 2014;127(16):2977-2981:10.3760/cma.j.issn.0366-6999.20140780...... miRNA functional inhibition assay Anti-miR miRNA antagonist for miR-21 (Ambion/Life Technologies, Grand Island, NY, USA) was transfected into H9c2(2-1) cells using iFect transfection kit (Neuromics, Edina, MN, USA) according to the manufacturers manual ...
The point was strictly obiter, because Pfizer did not in fact make any such argument; it simply contested the very hypothetical relied on by Teva, with the result that the burden remained with Teva [66]. However, the issue was fully considered, including reliance on the SCC decision in Rainbow Caterers [1991] 3 SCR 3, and the remark regarding Pfizers burden to prove an alternative hypothetical was made in the context of explaining why the burden remained with Teva in the context of the arguments made in this case [58]-[66]. The point was certainly more fully reasoned than the brief and somewhat cryptic discussion of this issue in Lovastatin [93]-[95]. Moreover it was expressly stated as a general principle of law, rather than, as in Lovastatin, a finding on the facts. It would seem to follow that this statement from Venlafaxine s8 FCA now represents the law on this point. ...
Lovastatin Lactone Diol ;. Simvastatin Lactone Diol ;. Monacolin J ;. 6(R)-[2-(8(S)-Hydroxy]-2(S),6(R)-dimethyl-1,2,6,7,8,8a(R)-hexahydro-1(S)-naphthyl]ethyl-4(R)-hydroxy-3,4,5,6-tetrahydro-2H-pyran-2-one ;. CAS # 79952-42-4 ;. C19H28O4 ;. MW: 320.42 ;. ...
Lovastatin (75330-75-5) Blocks cholesterol and isoprenoid biosynthesis via inhibition of HMG-CoA reductase (Ki=1nM for acid form).1,2 Induces apoptosis in various cell lines.3 Causes cell cycle arrest in early G1 phase.4 ...
I havent looked at the VIX for a while, but this 3 linear regression study (30,11,3) of the weekly bars gives something to ponder. Given the upslope of the VIX since the beginning of 2007, the 30 bar channel has been a good overbought/oversold tell. Disregarding the current oversold character of the markets, the position of the current VIX bar suggests that increased volatility is the likely trend for the near term. Based on the 3 LRs model, a reversion to the mean would take the VIX to the 27.50 area. . which would translate to a significant decline from current market levels. This concept is at odds with my previous VIX trading methodology which revolved around the VIXs propensity to revert at least 50% back towards the mean within 4 days. . .the mean being the 10 and 20 day SMAs. . when an 18% boundary had been violated. Although that system worked well going into late summer (82% reliable for the IWM)), the August and November performance was rather pitiful as the inverse correlation ...
Why then are we "down on Merck?" Merck manufactures a brand drug called Zocor, which is a member of the family called "statins" (I take a generic form of one of them, Mevacor, which is lovastatin) which act on the liver in such a way as to limit the production of cholesterol, which in the blood stream can theoretically deposit as "plaque" on the sides of arteries and narrow the opening of these vessels for the flow of blood and thereby cause heart attacks and strokes. I use the term "theoretically," because there is no cause-effect proven action between serum cholesterol in the blood and cholesterol from ruptures in plaque causing heart attacks and strokes. The connection seems obvious and likely, but other factors in the "statins" may also inhibit cardiovascular catastrophes: statins reduce a form of inflammation in the system on which medical research is still tilling the ground. But this reduction of "inflammation" may be more related to the statistical lowering of early death rates due to ...
Lovastatin used to lower cholesterol also lowers the levels of CoQ10 which would induce a new risk of cardiac disease. Supplementation of CoQ10 increased blood levels of CoQ10 and was generally accompanied by an improvement in cardiac function (Folkers K, et al. 1990 ...
GlaxoSmithKline (GSK) and Merck of Whitehouse Station, N.J., haveentered into an agreement for over-the-counter (OTC) marketing rightsfor Mevacor (lovastatin).
The amino acid leucine is efficiently used by the trypanosomatid Leishmania mexicana for sterol biosynthesis. The incubation of [2-13C]leucine with L. mexicana promastigotes in the presence of ketoconazole gave 14-methylergosta-8,24(241)-3-ol as the major sterol, which was shown by mass spectrometry to contain up to six atoms of 13C per molecule. 13C NMR analysis of the 14-methylergosta-8,24(241)-3-ol revealed that it was labeled in only six positions: C-2, C-6, C-11, C-12, C-16, and C-23. This established that the leucine skeleton is incorporated intact into the isoprenoid pathway leading to sterol; it is not converted first to acetyl-CoA, as in animals and plants, with utilization of the acetyl-CoA to regenerate 3-hydroxy-3-methylglutaryl-CoA (HMG-CoA). An inhibitor of HMG-CoA synthase (L-659,699) blocked the incorporation of [1-14C]acetate into sterol but had no inhibitory effect on [U-14C]leucine incorporation. The HMG-CoA reductase inhibitor lovastatin inhibited promastigote growth and ...
A kinetic model to describe lovastatin biosynthesis by Aspergillus terreus ATCC 20542 in a batch culture with the simultaneous use of lactose and glycerol as carbon sources was developed. In order to do this the kinetics of the process was first studied. Then, the model consisting of five ordinary differential equations to balance lactose, glycerol, organic nitrogen, lovastatin and biomass was proposed. A set of batch experiments with a varying lactose to glycerol ratio was used to finally establish the form of this model and find its parameters. The parameters were either directly determined from the experimental data (maximum biomass specific growth rate, yield coefficients) or identified with the use of the optimisation software. In the next step the model was verified with the use of the independent sets of data obtained from the bioreactor cultivations. In the end the parameters of the model were thoroughly discussed with regard to their biological sense. The fit of the model to the ...
Apomine, a 1,1-bisphosphonate-ester with antitumor activity, has previously been reported to strongly down-regulate 3-hydroxy-3-methylglutaryl-coenzyme A reductase (HMG-CoA reductase), the rate-limiting enzyme in the mevalonate pathway responsible for the prenylation of proteins. Here, we show that although apomine down-regulated HMG-CoA reductase protein levels in myeloma cells, it did not inhibit protein prenylation, and apomine-induced apoptosis could not be prevented by mevalonate, indicating that apomine cytotoxicity is independent from its effects on HMG-CoA reductase. Instead, apomine cytotoxicity was prevented by the addition of phosphatidylcholine, which is similar to the previously reported ability of phosphatidylcholine to overcome the cytotoxicity of farnesol, whereas phosphatidylcholine had no effect on down-regulation of HMG-CoA reductase by apomine. These findings raised the possibility that apomine, independent from its own cytotoxic effects, could enhance the antitumor effects of the
Our results demonstrate an interaction between lovastatin and paclitaxel in several cellular processes. In both the K562 and HL-60 cell lines, lovastatin was found to enhance paclitaxel-induced cytotoxicity in a synergistic manner (Fig. 1 and 2). In addition, lovastatin enhanced paclitaxel-induced G2-M arrest in both cell lines and paclitaxel-induced apoptosis in the HL-60 cells (Fig. 3-5). These interactions were not attributable to an effect by lovastatin on cellular paclitaxel levels (Fig. 6) or to a general effect by paclitaxel on isoprenylated proteins (Fig. 7). However, we found evidence to suggest that alterations in the expression of the isoprenylated centromere-associated protein mitosin might be involved (Fig. 8 and 9).. Because of a report that indicated that paclitaxel could alter protein isoprenylation (26), we investigated the effects of lovastatin and/or paclitaxel treatment on several isoprenylated proteins. Importantly, we found no evidence to suggest that paclitaxel alters ...
PubMed journal article HMG CoA reductase inhibitors (statins) for kidney transplant recipient were found in PRIME PubMed. Download Prime PubMed App to iPhone or iPad.
The purpose of this study is to evaluate and compare the relative bioavailability and therefore the bioequivalence of a test formulation of Lovastatin tablets to an equivalent dose of Mevacor® tablets after a single oral dose administered under fed conditions.. Fifty-four healthy, light/non/or ex-smoking, non-obese, male volunteers at least 18 years of age will be randomly assigned in a crossover fashion to receive each of two Lovastatin dosing regimens in sequence with a 7 day washout period between dosing periods. On the morning of Day 1, after an overnight fast of at least 10 hours, subjects will receive a standardized high-fat, high-calorie meal 30 minutes before drug administration. Thirty minutes after the start of the breakfast, a single oral dose of either the test formulation, Lovastatin (1 x 40 mg tablet), or a single oral dose of the reference formulation, Mevacor® (1 x 40 mg tablet) will be administered. After a 7 day washout period, on the morning of Day 8, following an overnight ...
Statins are among the most widely prescribed drugs worldwide. Numerous studies have shown their beneficial effects in prevention of cardiovascular disease through cholesterol-lowering and anti-atherosclerotic properties. Although some statin patients may experience muscle-related symptoms, severe side effects of statin therapy are rare, primarily due to extensive first-pass metabolism in the liver. Skeletal muscles appear to be the main site of side effects; however, recently some statin-related adverse effects have been described in tendon. The mechanism behind these side effects remains unknown. This is the first study that explores tendon-specific effects of statins in human primary tenocytes. The cells were cultured with different concentrations of lovastatin for up to 1 week. No changes in cell viability or morphology were observed in tenocytes incubated with therapeutic doses. Short-term exposure to lovastatin concentrations outside the therapeutic range had no effect on tenocyte viability;
The short-term lovastatin treatment did not induce muscle mass loss, muscle fiber atrophy, or creatine kinase (CK) release. It had no functional impact on slow-twitch Sol muscles. However, subtetanic stimulations at 10 Hz provoked greater force production in fast-twitch EDL muscles. The treatment also decreased the maximal rate of force development (dP/dT) of twitch contractions and prolonged the half relaxation time (1/2RT) of tetanic contractions of EDL muscles.. CONCLUSIONS ...
Almonds (lightly roasted) 1 oz 1.0 mg. Literature: Cholesterol:. Niacin is used in the treatment of hypercholesterolemia. The efficacy and safety of lovastatin and niacin were compared in a controlled, randomized, open-label study of a 26 week duration in 136 patients with primary hypercholesterolemia. Lovastatin and niacin both exerted favorable dose-dependent changes on the concentrations of plasma lipids and lipoproteins. Lovastatin was more effective in reducing LDL cholesterol concentrations, whereas niacin was more effective in increasing high-density lipoprotein cholesterol concentrations and reducing the Lp(a) lipoprotein level. Lovastatin was better tolerated than niacin, in large part because of the common cutaneous side effects of niacin. The dosages used were lovastatin 20mg/d and niacin 1.5 g/d for 10 weeks. Similar results were seen in another study where the two drugs reduced low-density lipoprotein-high-density lipoprotein ratios to a similar level, although these effects were ...
Almonds (lightly roasted) 1 oz 1.0 mg. Literature: Cholesterol:. Niacin is used in the treatment of hypercholesterolemia. The efficacy and safety of lovastatin and niacin were compared in a controlled, randomized, open-label study of a 26 week duration in 136 patients with primary hypercholesterolemia. Lovastatin and niacin both exerted favorable dose-dependent changes on the concentrations of plasma lipids and lipoproteins. Lovastatin was more effective in reducing LDL cholesterol concentrations, whereas niacin was more effective in increasing high-density lipoprotein cholesterol concentrations and reducing the Lp(a) lipoprotein level. Lovastatin was better tolerated than niacin, in large part because of the common cutaneous side effects of niacin. The dosages used were lovastatin 20mg/d and niacin 1.5 g/d for 10 weeks. Similar results were seen in another study where the two drugs reduced low-density lipoprotein-high-density lipoprotein ratios to a similar level, although these effects were ...
Immuno-oncology not only refers to the multifaceted relationship between our immune system and a developing cancer but also includes therapeutic approaches that harness the bodys immune system to fight cancer. The recognition that metabolic reprogramming governs immunity was a key finding with important implications for immuno-oncology. In this review, we want to explore how activation and differentiation-induced metabolic reprogramming affects the mevalonate pathway for cholesterol biosynthesis in immune and cancer cells. Glycolysis-fueled mevalonate metabolism is a critical pathway in immune effector cells, which may, however, be shared by cancer stem cells, complicating the development of therapeutic strategies. Additional engagement of fatty acidy oxidation, as it occurs in regulatory immune cells as well as in certain tumor types, may influence mevalonate pathway activity. Transcellular mevalonate metabolism may play an as yet unanticipated role in the crosstalk between the various cell types and
This compared the efficacy of HMG CoA reductase inhibitors + niacin vs HMG CoA reductase inhibitors in treating atherosclerosis in elderly patients.
New Targets of HMG-CoA Reductase Inhibitors (Statins) in the Central Nervous System. Statins are potent inhibitors of the hydroxymethylglutaryl-coenzyme A (HMG-CoA) reductase a key enzyme of the cellular cholesterol synthesis. They can induce comparatively large reductions in plasma cholesterol levels and are well proven drugs for the treatment of hypercholesterolaemia. Although the pharmacology of statins is well established for the peripheral system, data about their effects in the central nervous system (CNS) are still lacking. Clinical and epidemiological findings indicate prevention of stroke and possibly a beneficial effect on the progression of Alzheimers Disease (AD). Hence, statins are considered a promising drug in the CNS. Abnormal processing of amyloid precursor protein (APP) in the AD brain results in deposits of neurotoxic ß-amyloid (Aß) that represents one pathological hallmark of this disease. Statins lower the amyloidogenic processing of APP in vitro and in vivo. This effect ...
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The aim of this work was to investigate the role of CFTR in the control of AVD during STS-induced apoptosis. This objective has been guided by our preceding works demonstrating that CFTR is involved in lovastatin-induced apoptosis (4) and also in the control of RVD (3). Because similarities exist between RVD and AVD, it has been postulated that Cl− and K+ channels involved in both processes could be the same (31). Interestingly, in cultured mouse proximal cells, we have previously found that the TASK2 K+ channel could be the main K+ channel involved in STS-induced AVD (22). Moreover, CFTR and TASK2 are also implicated in the RVD process (3, 5). Based on these observations, we have raised the hypothesis that the involvement of CFTR in apoptosis could be due to the control of AVD. For this purpose, we used two different apoptosis inducers, STS and TNF-α. STS has severe toxic effects on renal cells and primarily mediates mitochondrial apoptosis, whereas TNF-α is an inflammatory cytokine that ...
The concept of phenologs. (Figure 1B in the PNAS paper.). In one practical example from the paper, known gene-phenotype associations from yeast were compared with known gene-phenotype associations from mice, using information from publicly available yeast and mouse genome databases. This showed that many genes that are associated with abnormal angiogenesis in mice have orthologous genes in yeast. Of course yeast doesnt have a circulation system, so these genes cant possibly be associated with angiogenesis in yeast, and indeed theyre not: In yeast, these same genes are involved in sensitivity to the hypercholesterolemia drug lovastatin. This suggests that lovastatin sensitivity in yeast could be a model for angiogenesis in vertebrates. To prove this, follow-up experiments showed that the transcription factor SOX13, which was identified as lovastatin-sensitive in yeast, is required for vascular development in Xenopus. Even more surprising than finding angiogenesis genes in yeast, is that a ...
Most discussions about using statin drugs focus on a 5-10 year period. Thats not the right way to discuss these drugs. When we take a statin drug (or screen for cancer, or any other preventive intervention) we do it to live longer-not just 5-10 years.. Here is a link to the (free) study. The editorial is here.. Researchers from the UK used national registries to calculate death rates. They then devised a mathematical model to calculate the probability distribution of lifespan gains from statin interventions. They used the well-accepted relative (CV) benefits of statins of 20-30%. In the third part of the study, they surveyed random people in train stations, asking how they would judge potential benefit from the drugs.. Before I tell you the results, lets consider how we currently explain statin benefits. In primary prevention, the absolute benefit from a statin drug (or cancer screening) is small. How small is a matter of debate, but what opponents to these therapies rightly say is that most ...
Press releases and media reports about statin drugs often dramatically overstate their effectiveness, while understating their risk.I just read a fantastic article by Dr. Malcolm Kendrick about how deceptive and misleading media reporting on statin drug trials can be.But thats not what the study showed at all. In fact, the following would be a more accurate report on the results of this study, couched in the context of what we know from other statin drug trials:Out of 100 high-risk people taking a statin for five years, 98.2 will not benefit at all-but they will be exposed to significant side effects and complications, including muscle damage and diabetes. The 1.8 people that do benefit will live an average of 6 months (and a maximum of one year) longer than those that didnt take the statin. These results only apply to the people at highest risk for a future heart attack: middle-aged men whove already had a heart attack (aka
Rashid, S.A.,Ibrahim D., & Aryantha, I.N.P., 2013, Effect Of Cultural Conditions On Lovastatin Production By Aspergillus Niger Sar I Using Combination Of Rice Bran And Brown Rice As Substrate, International Journal of Applied Biology and Pharmaceutical Technology, 4(2) : 150- ...
New research has shown that statins, one of the most commonly prescribed cardiovascular drugs worldwide, may reduce the positive effects of exercise in overweight individuals. Statins are primarily prescribed to lower elevated LDL cholesterol levels, but may be recommended for patients as a preventative health measure if they are deemed to be at risk of metabolic syndrome, or obese. Statin drugs are already associated with a range of debilitating side effects including moderate or serious liver dysfunction, acute renal failure, moderate or serious myopathy (muscle disease), and cataracts.. It seems ironic that they may also hinder the ability of exercise to improve fitness levels and health in the people that need it most - thereby worsening the very conditions they are supposed to treat. While this study was conducted on a small population of sedentary overweight and obese adults, clinically significant differences in cardiorespiratory fitness were reported in patients taking statin drugs ...
This invention relates to a novel process for the preparation of 3-hydroxy-3-methylglutarylcoenzyme A (HMG-CoA) reductase inhibitors which contain a 4-hydroxy-3,4,5,6-tetrahydro-2H-pyran-2-one moiety, such as compactin and mevinolin, by utilizing an alkyl 4-cyano-3(R)-hydroxybutanoate as a chiral synthon for the stereospecific introduction of the 4-hydroxy-3,4,5,6-tetrahydro-2H-pyran-2-one moiety.
At any time, you can complete this interactive online quiz to check how well you understand using linear regression. Print off the worksheet if you...
Riva-Atorvastatin: Atorvastatin belongs to the group of medications known as HMG CoA reductase inhibitors (statins) or lipid metabolism regulators. It is used to treat people who have high cholesterol levels, including those people who have certain inherited cholesterol disorders. When you use this medication, you also need to make lifestyle changes, including switching to a diet low in fat and cholesterol, quitting smoking, and increasing the amount of exercise you do.
Crestor: Rosuvastatin belongs to the group of medications known as HMG CoA reductase inhibitors (statins). It is used, along with a healthy diet and exercise program, to improve cholesterol levels by lowering bad cholesterol and raising good cholesterol. It is also used to treat people who have certain inherited cholesterol disorders.
Mylan-Rosuvastatin: Rosuvastatin belongs to the group of medications known as HMG CoA reductase inhibitors (statins). It is used, along with a healthy diet and exercise program, to improve cholesterol levels by lowering bad cholesterol and raising good cholesterol. It is also used to treat people who have certain inherited cholesterol disorders.
pms-Atorvastatin: Atorvastatin belongs to the group of medications known as HMG CoA reductase inhibitors (statins). It is used to treat people who have high cholesterol levels, including those people who have certain inherited cholesterol disorders. When you use this medication, you also need to make lifestyle changes, including switching to a diet low in fat and cholesterol, quitting smoking, and increasing the amount of exercise you do.
My sister-in-law (doctor) applauded my desire to lose weight, but she was really concerned when she read my blood pressure. My doctor was monitoring it at the beginning of this year and prescribed Lisinopril 20mg daily. Lisinopril is standard treatment for patients with high blood pressure (hypertension) and considering that my BP was clearly in the 140/90 range on a daily basis, this treatment was recommended for 120 days. He also prescribed Lovastatin 20mg for the treatment of high cholesterol. It is sold under the brand name Mevacor® but is also available as a generic called Lovastatin tablets. He wanted to reduce my LDL cholesterol levels into a normal range. This treatment lasted 90 days, which ended about 15 days ago. ...
Learn more about Statin Drugs at Grand Strand Medical Center Type of Medication 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA)...
Learn more about Statin Drugs at Regional Medical Center Bayonet Point Type of Medication 3-hydroxy-3-methylglutaryl coenzyme...
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This topic contains 451 study abstracts on Statin Drugs indicating they may contribute to Statin-Induced Pathologies, Myopathies, and Chemically-Induced Liver Damage
by Dr John Briffa The Cholesterol Truth Excerpts: When drug company PR extols the virtues of statin drugs, statistics will invariably be presented which make
Information on potential interactions and warnings of Statin Drugs such as lipitor, zocor, altocor, baycol, rosuvastatin and mevachor.
Statin drugs are a popular way for people to lower their risks of heart attack and stroke, and they are sold under different names and dosages.
Originally Posted by EnigmaO01 No worries. I am seeing a good physician. Hes the one that suggested we stop the statin drug for a month to see what
Revised guidelines for statin therapy focus on the cholesterol-lowering drugs' ability to prevent heart attacks and strokes.
Downloadable! This paper provides a simple method to account for heteroskedasticity and cross-sectional dependence in samples with large cross sections and relatively few time-series observations. The method is motivated by cross-sectional regression studies in finance and accounting. Simulation evidence suggests that these estimators are dependable in small samples and may be useful when generalized least squares is infeasible, unreliable, or computationally too burdensome. We also consider efficiency issues and show that, in principle, asymptotic efficiency can be improved using a technique due to Cragg (1983).
My research is mainly focused on the effects of cholesterol, saturated fat and statin drugs on health. If you know anyone who is worried about their cholesterol levels and heart disease, or has been told to take statin drugs you could send them a link to this website, and to my statin or cholesterol or heart disease books ...
Mevacor: Lovastatin belongs to the family of medications known as lipid metabolism regulators. It is used in addition to diet and exercise to lower high cholesterol. It is also used to slow the progression of coronary atherosclerosis (hardening of the arteries in the heart). It works by blocking an enzyme that is needed to make cholesterol in the body. Less cholesterol is made, and cholesterol levels in the blood decrease.
Riva-Lovastatin: Lovastatin belongs to the family of medications known as lipid metabolism regulators. It is used in addition to diet and exercise to lower high cholesterol. It is also used to slow the progression of coronary atherosclerosis (hardening of the arteries in the heart). It works by blocking an enzyme that is needed to make cholesterol in the body. Less cholesterol is made, and cholesterol levels in the blood decrease.
Atorvastatin (Lipitor, Torvast)Fluvastatin (Lescol, Lescol XL)Lovastatin (Mevacor, Altocor)MevastatinPitavastatin (Livalo, Pitava)Pravastatin (Pravachol,
It will investigate the efficacy and pharmacodynamics of the drotrecogin-alfa, lovastatin drugs in volunteers. The primary outcome is [18F] fluorodeoxyglucose
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http://youtu.be/ip9eT8K8S4o By Dr. Mercola Statins are the worlds most-prescribed class of medications. A staggering one in four Americans over the age
Despite their success as multi-billion dollar cholesterol medications, statins have been shown to increase the risk of the neurodegenerative disease Parkinsons. The list of statin drug-induced disorders also includes diabetes, cataracts
A few months ago, I wrote an editorial for EmpowHER called Fish Oil vs. Statins: You be the Judge. I had just received results that my cholesterol and triglyceride levels had gone through the roof.
i have CAD, HBP, stents & had a heart attack, also have high colesterol 218, im 66. not active. my doc recently cut my chlosterol rx in half. what to do besides take nitro? barbara
DISCUSSION We are left with these facts about the use of statin drugs in adolescence: Statins are highly effective for the short-term lowering of
The danger of statins. Learn about alternatives to taking statins. According to a new theoretical study from the University of Oxford, eating one apple every day matches the vascular benefits of statin drugs without any of the harmful side effects.
If you take statin drugs without taking CoQ10, your health is at serious risk because there is mounting evidence of some 900 catastrophic side effects so far.
Like other statin drugs, adverse reactions can occur with the use of Pravachol. Some of them are minimal and mild, however other Pravachol side effects are
Researchers at UCLA wondered whether red yeast rice might also be useful for preventing cancer. We know that lovastatin decreases blood cholesterol, but it also has an anti-inflammation effect, and inflammation is a primary risk factor in colon cancer development, explains Mee Young Hong, MD, who was a research fellow in the UCLA Center for Human Nutrition when she worked on the study, and is now assistant professor at San Diego State University. We thought that red yeast rice, which contains a natural source of lovastatin, might help with cancer prevention. Past research has found that cancerous tumors need cholesterol to grow, and studies have shown that people who take statins have a reduced risk of colon cancer.. Dr. Hong and her colleagues compared the effects of different Chinese red yeast rice formulations with the drug lovastatin on colon cancer cells in a laboratory.* The red yeast rice triggered tumor cell death, and it reduced tumor cell growth by as much as 41%--an even greater ...
Another popular cholesterol-lowering supplement is red yeast rice. There is some evidence that red yeast rice can help lower your LDL cholesterol. However, the Food and Drug Administration has warned that red yeast rice products could contain a naturally occurring form of the prescription medication known as lovastatin.. Lovastatin in red yeast rice products is potentially dangerous because theres no way to know how much lovastatin might be in a particular product. And theres no way to determine the quality of the lovastatin. ...
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A method for converting compactin to pravastatin is described. Compactin is provided and contacted with an agent derived from Actinomadura under conditions in which the agent converts compactin to pravastatin. Also described are an Actinomadura strain, an Actinomadura cell free extract, an Actinomadura hydroxylase, and a method for lowering cholesterol levels in mammals.
High dose statins prevents dementia, study suggests - Science Daily, 8/31/13 - the current study examined whether statin use was associated with new diagnoses of dementia. The researchers used a random sample of 1 million patients covered by Taiwans National Health Insurance ... The adjusted hazard ratios (HRs) for dementia were significantly inversely associated with increased daily or total equivalent statin dosage. The HRs for the three tertiles of mean equivalent daily dosage (lowest to highest) were 0.622, 0.697 and 0.419 vs control ... Patients who received the highest total equivalent doses of statins had a 3-fold decrease in the risk of developing dementia ... Almost all the statins (except lovastatin) decreased the risk for new onset dementia when taken at higher daily doses. A high mean daily dosage of lovastatin was positively associated with the development of dementia, possibly because lovastatin is a lipophilic statin while the anti-inflammatory cholesterol lowering effect of ...
China 100% Natural Red Yeast Rice Extract: 0.4%-3% Lovastatin; 0.4%, 1.5% Monacolin K., Find details about China Red Yeast Rice Extract, Monascus Purpureus from 100% Natural Red Yeast Rice Extract: 0.4%-3% Lovastatin; 0.4%, 1.5% Monacolin K. - Kingherbs Limited
Background: 3-hydroxy-3-methylglutaryl-CoA reductase inhibitors (statins) reduce serum cholesterol, and cardiovascular morbidity and mortality. The role of lipids in the progression of kidney disease and the potential beneficial effects of statins on renal function is unknown. Oxidative stress and inflammation may be the missing link between CAD and chronic kidney disease. Statins may protect the kidney through both lipid lowering properties and pleiotropic effects.. Methods: We analyzed data in 197, 551 patients (mean age 64.8 ± 13.6 years, 95% males, 29.5% (58,332) statin users, and 70.5% (139, 219) non-statin users), who had baseline creatinine less than 3.5 mg/dl, from the cross-sectional data mined from the Veterans Affairs VISN 16 database. Deterioration of renal function was defined as doubling of the baseline or increase in creatinine of 0.5 mg/dl over at least 90 days.. Results: Based on this definition, 3.4% of patients developed renal deterioration over 5 year of follow-up. After ...
Red Yeast Rice (RYR) has been used for almost 2,300 years. It originated in China and has been used as both a food coloring and a medicinal herb. In around 800 AD in China, it was taken internally to "invigorate the body, aid in digestion and revitalize the blood". RYR has also been used in Traditional Chinese Medicine (TCM) to help the spleen, eliminate phlegm, and improve blood circulation. In Japan, Red Yeast Rice is called hoji, which translates to "grain or bean overgrown with mold". RYR is made by fermenting rice with a species of yeast known as Monascus purpeus and contains compounds called monacolins. These chemicals inhibit the production of an enzyme doctors call "HMG-CoA reductase", which when blocked, stops the body from producing cholesterol. In the 1970s, Merck & Company scientists isolated the chemical monacolin K. Shortly after, they learned how to synthesize this chemical in the lab. They called it Lovastatin (Mevacor, Altoprev, Altocor), a drug that would forever change the way ...
One of the main objectives of this study is to further examine the contributory roles of protein farnesylation and geranylgeranylation in glucose- and calcium-induced insulin secretion from isolated β cells. Our data clearly support original observations from our laboratory (Metz et al., 1993) and those of others (Li et al., 1993) suggesting that isoprenylation steps are critical to physiological insulin secretion. To the best of our knowledge, there have been only two studies that examined the contributory roles of protein isoprenylation in insulin secretion. Using LOVA, Li et al. (1993) first reported that inhibition of isoprenylation resulted in significant attenuation in bombesin and vasopressin potentiation of nutrient-induced insulin secretion from HIT-T15 cells. These investigators have also provided evidence to indicate abnormalities in subcellular distribution (i.e., significant accumulation of unprenylated proteins in the cytosolic fraction) of small G proteins in LOVA-treated cells. ...
Red yeast rice (Monascus purpureus), a traditional Chinese medication, has been used for many years to effectively lower cholesterol.1,2 As a natural alternative to treat dyslipidemia, red yeast rice has the same chemical identity as lovastatin.1 Lovastatin along with the other HMG Co-A reductase inhibitors (statins) have been associated with statin-associated myopathy (SAM). This clinical syndrome can occur in 5% to 10% of statin users.2,3 Myopathy may be further categorized as myalgias (muscle pain), myositis (enzyme leak with increased creatine kinase levels), or rhabdomyolysis (creatine kinase elevations >10,000 u/L associated with acute renal failure). There is no consensus on how to treat dyslipidemias in patients who cannot tolerate statin therapy due to SAM. While, red yeast rice has been associated with the development of symptomatic myopathies only in case reports, it is perceived by some to be a "real" alternative to statin therapy.4 A recent clinical trial evaluated the effectiveness ...
To this day, even as Big Pharma continues to explore Traditional Chinese Medicine for its goldmine of treatments and cures, the entire western medical system routinely attacks Chinese Medicine and says its all hokum. But once they find a molecule that can earn them billions of dollars, suddenly its heralded as "scientific medicine!" …but only with the brand name, not the original plant name from which it was derived.. Statin drugs, the best-selling pharmaceuticals on the market today, were derived from lovastatin molecules naturally found in red yeast rice. After pirating these molecules from nature and patenting their variations, the drug industry urged the FDA to attack red yeast rice supplements, calling them "adulterated" because they contained lovastatin molecules. The FDA then warned the public that red yeast rice was adulterated with pharmaceuticals.. This is the scam of western medicine: You are told by "scientific experts" that plants, herbs, mushrooms and nutrients are worthless ...
Currently, statins are the only drugs acting on the mammalian isoprenoid pathway. The mammalian genes in this pathway are not easily amenable to genetic manipulation. Thus, it is difficult to study the effects of the inhibition of various enzymes on the intermediate and final products in the isoprenoid pathway. In fission yeast, antifungal compounds such as azoles and terbinafine are available as inhibitors of the pathway in addition to statins, and various isoprenoid pathway mutants are also available. Here in these mutants, treated with statins or antifungals, we quantified the final and intermediate products of the fission yeast isoprenoid pathway using liquid chromatography-mass spectrometry/mass spectrometry. In hmg1-1, a mutant of the gene encoding 3-hydroxy-3-methylglutaryl coenzyme A reductase (HMGR), ergosterol (a final sterol product), and squalene (an intermediate pathway product), were decreased to approximately 80% and 10%, respectively, compared with that of wild-type cells. Consistently

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Lovastatin 20 mg q.p.m. (N = 1642) % Lovastatin 40 mg q.p.m. (N = 1645) % Lovastatin 20 mg b.i.d. (N = 1646) % Lovastatin 40 mg ... Lovastatin acid refers to the β-hydroxyacid of lovastatin. ‡ The mean total AUC of lovastatin without itraconazole phase could ... TABLE II Lovastatin vs. Placebo(Mean Percent Change from Baseline After 6 Weeks) DOSAGE N TOTAL-C LDL-C HDL-C LDL-C/ HDL-C ... TABLE III Lovastatin vs. Cholestyramine(Percent Change from Baseline After 12 Weeks) TREATMENT N TOTAL-C (mean) LDL-C (mean) ...
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Differential Effects of Lovastatin on the Trafficking of Endogenous and Lipoprotein-Derived Cholesterol in Human Monocyte...Differential Effects of Lovastatin on the Trafficking of Endogenous and Lipoprotein-Derived Cholesterol in Human Monocyte...

In nonloaded cells, lovastatin produced a significant decrease in total cholesterol levels (−18% at 12 μmol/L lovastatin, P, ... P,0.01, **P,0.001 lovastatin treated versus untreated; §P,0.001 untreated, secretion versus loading; and #P,0.001 lovastatin ... was reduced by lovastatin (Figure 4⇓). Because ACAT activity in lovastatin-treated cells appears to be normal (Figure 3⇑), and ... at 12 μmol/L lovastatin (Figure 1⇓). By contrast, cholesteryl esters increased 2.2-fold in the presence of 12 μmol/L lovastatin ...
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Lovastatin; 0.4%, 1.5% Monacolin K., Find details about China Red Yeast Rice Extract, Monascus Purpureus from 100% Natural Red ... Yeast Rice Extract: 0.4%-3% Lovastatin; 0.4%, 1.5% Monacolin K. - Kingherbs Limited ... NLT 3.0% Lovastatin. 3.07%. HPLC. Loss on Drying. NMT 10%. 6.12%. 5g / ... Specification: 0.4%-3% Lovastatin;. 0.4%, 1.5% Monacolin K& ...
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Upregulation of Endothelial Nitric Oxide Synthase by HMG CoA Reductase Inhibitors | CirculationUpregulation of Endothelial Nitric Oxide Synthase by HMG CoA Reductase Inhibitors | Circulation

Again, ox-LDL decreased steady-state ecNOS mRNA by 52±5% after 24 hours (P,.01, n=3) (Fig 2B⇑). Treatment with lovastatin (10 ... Treatment with lovastatin alone, however, produced 36% increase in ecNOS mRNA levels compared with untreated cells (P,.05, n=3 ... Simvastatin and lovastatin were obtained from Merck, Sharp, and Dohme, Inc. Because endothelial cells lack lactonases to ... A, Time-dependent effects of simvastatin (Sim, 0.1 μmol/L). B, Effects of lovastatin (Lov, 10 μmol/L) after 24 hours. Each ...
more infohttp://circ.ahajournals.org/content/97/12/1129

Trends in the Use of Nonstatin Lipid-Lowering Therapy Among Patients With Coronary Heart Disease | JACC: Journal of the...Trends in the Use of Nonstatin Lipid-Lowering Therapy Among Patients With Coronary Heart Disease | JACC: Journal of the...

Seven statins were studied (atorvastatin, fluvastatin, lovastatin, pitavastatin, pravastatin, rosuvastatin, and simvastatin). ...
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Red Yeast Rice, the Real Statin | Topics in Evidence-Based Pharmacy Practice | AccessPharmacy | McGraw-Hill MedicalRed Yeast Rice, the "Real" Statin | Topics in Evidence-Based Pharmacy Practice | AccessPharmacy | McGraw-Hill Medical

... red yeast rice has the same chemical identity as lovastatin.1 Lovastatin along with the other HMG Co-A reductase inhibitors ( ...
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They called it Lovastatin (Mevacor, Altoprev, Altocor), a drug that would forever change the way doctors treated high ... The first blockbuster cholesterol-lowering drug, known as Lovastatin (Mevacor), was released in 1987. Over the next decade, ...
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The naturally occurring lovastatins and analogs are called monacolins K, L, J, and also occur in their hydroxyl acid forms ... The prescription drug lovastatin, identical to monacolin K, is the principal statin produced by M. purpureus. Only the open- ...
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Niacin/lovastatin (trade names Advicor, Mevacor) is a drug combination used for the treatment of dyslipidemia. It is a ... combination of the vitamin niacin and the statin drug lovastatin. The combination preparation is marketed by Abbott ... Retrieved from "https://en.wikipedia.org/w/index.php?title=Niacin/lovastatin&oldid=775316315" ...
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A list of US medications equivalent to Lovastatin Domesco is available on the Drugs.com website. ... Lovastatin Domesco is a medicine available in a number of countries worldwide. ... Ingredient matches for Lovastatin Domesco. Lovastatin. Lovastatin is reported as an ingredient of Lovastatin Domesco in the ... Lovastatin Domesco. Lovastatin Domesco may be available in the countries listed below. ...
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... lovastatin, gluten free - Additional details: I am a celiac and need to be sure that there is no more gluten in each tablet ... Home › Q & A › Questions › Is Lovastatin gluten free?. Is Lovastatin gluten free?. Asked. 1 Jun 2016 by Anonymous. Topics. ... lovastatin, gluten free. Details:. I am a celiac and need to be sure that there is no more gluten in each tablet than are ... Side Effects of Lovastatin (detailed). Search for questions. Still looking for answers? Try searching for what you seek or ask ...
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Large-scale trials confirmed the effectiveness of lovastatin. Observed tolerability continued to be excellent, and lovastatin ... "Lovastatin Pregnancy and Breastfeeding Warnings". Drugs.com. Retrieved 3 March 2019.. *^ Fischer, Jnos; Ganellin, C. Robin ( ... "Grapefruit juice greatly increases serum concentrations of lovastatin and lovastatin acid". Clin Pharmacol Ther. 63 (4): 397- ... Lovastatin was patented in 1979 and approved for medical use in 1987.[4] It is available as a generic medication.[2] In the ...
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LOVASTATIN (LOE va sta tin) is known as a HMG-CoA reductase inhibitor or statin. It lowers the level of cholesterol in the ... Highlights for lovastatin. Oral tablet. 1 LOVASTATIN (LOE va sta tin) is known as a HMG-CoA reductase inhibitor or statin. It ... lovastatin Side Effects. Oral tablet. Side effects that you should report to your doctor or health care professional as soon as ... How to Use lovastatin Oral tablet. Take this medicine by mouth with a glass of water. Follow the directions on the prescription ...
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Lovastatin differs structurally from mevastatin by a single methyl group at the 6 position. Lovastatin is a prodrug that is ... Japan) patented lovastatin isolated from Monascus ruber four months before Merck. Lovastatin was found to be 2 times more ... Lovastatin is a competitive inhibitor of HMG-CoA reductase with a binding affinity 20,000 times greater than HMG-CoA. ... Like mevastatin, lovastatin is structurally similar to hydroxymethylglutarate (HMG), a substituent of HMG-Coenzyme A (HMG-CoA ...
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Lovastatin decreases coenzyme Q levels in humans. | PNASLovastatin decreases coenzyme Q levels in humans. | PNAS

The clinical use of lovastatin is to reduce a risk of cardiac disease, and if lovastatin were to reduce levels of CoQ10, this ... Lovastatin decreases coenzyme Q levels in humans.. K Folkers, P Langsjoen, R Willis, P Richardson, L J Xia, C Q Ye, H Tamagawa ... Lovastatin decreases coenzyme Q levels in humans.. K Folkers, P Langsjoen, R Willis, P Richardson, L J Xia, C Q Ye, H Tamagawa ... Lovastatin decreases coenzyme Q levels in humans.. K Folkers, P Langsjoen, R Willis, P Richardson, L J Xia, C Q Ye, and H ...
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Lovastatin (Mevacor, Altoprev): Cholesterol Drug Dosage & Side EffectsLovastatin (Mevacor, Altoprev): Cholesterol Drug Dosage & Side Effects

Lovastatin should be used in addition to dietary modifications as part of a treatment plan to lower cholesterol levels when the ... Lovastatin is a cholesterol-lowering medication called a statin prescribed to treat elevated blood cholesterol levels. ... Generic Name: Lovastatin. Drug Class: Lipid-Lowering Agents, Statins; HMG-CoA Reductase Inhibitors. What Is Lovastatin Used For ... This medication contains lovastatin. Do not take Mevacor or Altoprev if you are allergic to lovastatin or any ingredients ...
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Ran-Lovastatin synonyms, Ran-Lovastatin pronunciation, Ran-Lovastatin translation, English dictionary definition of Ran- ... Lovastatin. n. A statin drug, C24H36O5, that blocks the bodys synthesis of cholesterol and is used to lower cholesterol levels ... lovastatin. (redirected from Ran-Lovastatin). Also found in: Thesaurus, Medical. lo·va·stat·in. (lō′və-stăt′n). n.. A statin ... Ran-Lovastatin - definition of Ran-Lovastatin by The Free Dictionary https://www.thefreedictionary.com/Ran-Lovastatin ...
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Interactions between Lovastatin Oral and atorvastatin-40mg-lovastatin-simvastatin-ciprofloxacinInteractions between Lovastatin Oral and atorvastatin-40mg-lovastatin-simvastatin-ciprofloxacin

WebMD provides information about interactions between Lovastatin Oral and atorvastatin-40mg-lovastatin-simvastatin- ... Drugs & MedicationsLovastatin. Atorvastatin (, 40mg): Lovastatin; Simvastatin/Ciprofloxacin Interactions. This information is ...
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Lovastatin Oral : Uses, Side Effects, Interactions, Pictures, Warnings & Dosing - WebMDLovastatin Oral : Uses, Side Effects, Interactions, Pictures, Warnings & Dosing - WebMD

Find patient medical information for Lovastatin Oral on WebMD including its uses, side effects and safety, interactions, ... Do not take any red yeast rice products while you are taking lovastatin since those products may also contain lovastatin. ... Other medications can affect the removal of lovastatin from your body, which may affect how lovastatin works. Examples include ... Before taking lovastatin, tell your doctor or pharmacist if you are allergic to it; or if you have any other allergies. This ...
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  • Lovastatin is a specific inhibitor of HMG-CoA reductase, the enzyme which catalyzes the conversion of HMG-CoA to mevalonate. (nih.gov)
  • Lovastatin is a lactone which is readily hydrolyzed in vivo to the corresponding β-hydroxyacid, a strong inhibitor of HMG-CoA reductase. (nih.gov)
  • Inhibition of HMG-CoA reductase is the basis for an assay in pharmacokinetic studies of the β-hydroxyacid metabolites (active inhibitors) and, following base hydrolysis, active plus latent inhibitors (total inhibitors) in plasma following administration of lovastatin. (nih.gov)
  • After oral ingestion, lovastatin, which is an inactive lactone, is hydrolyzed to the corresponding β-hydroxyacid form. (nih.gov)
  • Lovastatin has been shown to reduce elevated LDL-C concentrations. (nih.gov)
  • Plasma concentrations of total radioactivity (lovastatin plus 14 C-metabolites) peaked at 2 hours and declined rapidly to about 10% of peak by 24 hours postdose. (nih.gov)
  • In animal studies, after oral dosing, lovastatin had high selectivity for the liver, where it achieved substantially higher concentrations than in non-target tissues. (nih.gov)
  • In addition to the active ingredient lovastatin, each tablet contains the following inactive ingredients: D&C Yellow No. 10 Aluminum Lake, FD&C Blue No. 2 Aluminum Lake, lactose anhydrous, lactose monohydrate, magnesium stearate, microcrystalline cellulose and pregelatinized corn starch. (nih.gov)
  • The mechanism of the LDL-lowering effect of lovastatin may involve both reduction of VLDL-C concentration, and induction of the LDL receptor, leading to reduced production and / or increased catabolism of LDL-C. Apolipoprotein B also falls during treatment with lovastatin. (nih.gov)
  • Lovastatin undergoes extensive first-pass extraction in the liver, its primary site of action, with subsequent excretion of drug equivalents in the bile. (nih.gov)
  • The empirical formula of lovastatin is C 24 H 36 O 5 and its molecular weight is 404.55. (nih.gov)
  • Lovastatin tablets USP are supplied as 10 mg, 20 mg and 40 mg tablets for oral administration. (nih.gov)
  • Following an oral dose of 14 C-labeled lovastatin in man, 10% of the dose was excreted in urine and 83% in feces. (nih.gov)
  • Absorption of lovastatin, estimated relative to an intravenous reference dose, in each of four animal species tested, averaged about 30% of an oral dose. (nih.gov)
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