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.
Compounds that inhibit HMG-CoA reductases. They have been shown to directly lower cholesterol synthesis.
Substances used to lower plasma CHOLESTEROL levels.
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.
Phosphoric or pyrophosphoric acid esters of polyisoprenoids.
Enzymes that catalyze the reversible reduction of alpha-carboxyl group of 3-hydroxy-3-methylglutaryl-coenzyme A to yield MEVALONIC ACID.
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.
The principal sterol of all higher animals, distributed in body tissues, especially the brain and spinal cord, and in animal fats and oils.
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)
An antilipemic fungal metabolite isolated from cultures of Nocardia autotrophica. It acts as a competitive inhibitor of HMG CoA reductase (HYDROXYMETHYLGLUTARYL COA REDUCTASES).
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)
A genus in the family Monascaceae, order EUROTIALES. One species, Monascus purpureus, has multiple uses in traditional Chinese medicine (MEDICINE, CHINESE TRADITIONAL).
Highly crosslinked and insoluble basic anion exchange resin used as anticholesteremic. It may also may reduce triglyceride levels.
A genus of mitosporic fungi containing about 100 species and eleven different teleomorphs in the family Trichocomaceae.
Specific hydroxymethylglutaryl CoA reductases that utilize the cofactor NAD. In liver enzymes of this class are involved in cholesterol biosynthesis.
Fatty acids which are unsaturated in only one position.
Prolamins in the endosperm of SEEDS from the Triticeae tribe which includes species of WHEAT; BARLEY; and RYE.
A malabsorption syndrome that is precipitated by the ingestion of foods containing GLUTEN, such as wheat, rye, and barley. It is characterized by INFLAMMATION of the SMALL INTESTINE, loss of MICROVILLI structure, failed INTESTINAL ABSORPTION, and MALNUTRITION.
A diet which is devoid of GLUTENS from WHEAT; BARLEY; RYE; and other wheat-related varieties. The diet is designed to reduce exposure to those proteins in gluten that trigger INFLAMMATION of the small intestinal mucosa in patients with CELIAC DISEASE.
Simple protein, one of the prolamines, derived from the gluten of wheat, rye, etc. May be separated into 4 discrete electrophoretic fractions. It is the toxic factor associated with CELIAC DISEASE.
Rare, chronic, papulo-vesicular disease characterized by an intensely pruritic eruption consisting of various combinations of symmetrical, erythematous, papular, vesicular, or bullous lesions. The disease is strongly associated with the presence of HLA-B8 and HLA-DR3 antigens. A variety of different autoantibodies has been detected in small numbers in patients with dermatitis herpetiformis.
The middle portion of the SMALL INTESTINE, between DUODENUM and ILEUM. It represents about 2/5 of the remaining portion of the small intestine below duodenum.
Diseases of the peripheral nerves external to the brain and spinal cord, which includes diseases of the nerve roots, ganglia, plexi, autonomic nerves, sensory nerves, and motor nerves.
Peripheral, autonomic, and cranial nerve disorders that are associated with DIABETES MELLITUS. These conditions usually result from diabetic microvascular injury involving small blood vessels that supply nerves (VASA NERVORUM). Relatively common conditions which may be associated with diabetic neuropathy include third nerve palsy (see OCULOMOTOR NERVE DISEASES); MONONEUROPATHY; mononeuropathy multiplex; diabetic amyotrophy; a painful POLYNEUROPATHY; autonomic neuropathy; and thoracoabdominal neuropathy. (From Adams et al., Principles of Neurology, 6th ed, p1325)
A group of slowly progressive inherited disorders affecting motor and sensory peripheral nerves. Subtypes include HMSNs I-VII. HMSN I and II both refer to CHARCOT-MARIE-TOOTH DISEASE. HMSN III refers to hypertrophic neuropathy of infancy. HMSN IV refers to REFSUM DISEASE. HMSN V refers to a condition marked by a hereditary motor and sensory neuropathy associated with spastic paraplegia (see SPASTIC PARAPLEGIA, HEREDITARY). HMSN VI refers to HMSN associated with an inherited optic atrophy (OPTIC ATROPHIES, HEREDITARY), and HMSN VII refers to HMSN associated with retinitis pigmentosa. (From Adams et al., Principles of Neurology, 6th ed, p1343)
A branch of the tibial nerve which supplies sensory innervation to parts of the lower leg and foot.
The propagation of the NERVE IMPULSE along the nerve away from the site of an excitation stimulus.
Diseases of multiple peripheral nerves simultaneously. Polyneuropathies usually are characterized by symmetrical, bilateral distal motor and sensory impairment with a graded increase in severity distally. The pathological processes affecting peripheral nerves include degeneration of the axon, myelin or both. The various forms of polyneuropathy are categorized by the type of nerve affected (e.g., sensory, motor, or autonomic), by the distribution of nerve injury (e.g., distal vs. proximal), by nerve component primarily affected (e.g., demyelinating vs. axonal), by etiology, or by pattern of inheritance.
Foods and beverages prepared for use to meet specific needs such as infant foods.
A trace element that is required in bone formation. It has the atomic symbol Sn, atomic number 50, and atomic weight 118.71.
Works containing information articles on subjects in every field of knowledge, usually arranged in alphabetical order, or a similar work limited to a special field or subject. (From The ALA Glossary of Library and Information Science, 1983)
A triterpene that derives from the chair-boat-chair-boat folding of 2,3-oxidosqualene. It is metabolized to CHOLESTEROL and CUCURBITACINS.
A standardized nomenclature for clinical drugs and drug delivery devices. It links its names to many of the drug vocabularies commonly used in pharmacy management.
Component of the NATIONAL INSTITUTES OF HEALTH. Through basic and clinical biomedical research and training, it conducts and supports research with the objective of cancer prevention, early stage identification and elimination. This Institute was established in 1937.
Lists of words, usually in alphabetical order, giving information about form, pronunciation, etymology, grammar, and meaning.

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)

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 ...
The effect of lovastatin on serum lipids and its tolerability in patients with non-familial primary hypercholesterolemia (type II-A and type II-B) during a six-month period were evaluated in this open-label study. Thirty-eight patients were enrolled in the study; tolerability was assessed in all 38 patients. Thirty patients completed the study, and the effect of lovastatin on serum lipids in these patients was assessed. Some patients had been treated for hypercholesterolemia with long-term dietary and other non-pharmacologic means before entry into the study. All patients were unresponsive to a six-week program of intensive dietary therapy and other nonpharmacologic treatment to lower their blood cholesterol levels before receiving lovastatin. While maintaining intensive dietary therapy, administration of lovastatin was instituted at a dosage of 20 mg/day, which was increased by 20-mg increments monthly, as necessary, to a maximum of 80 mg/day. In an effort to achieve goal levels of low-density ...
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 ...
Several studies have shown that statins are not only lipid-lowering drugs, but also are potent modulators of the immune system (16). Given the broad administration of these drugs in the population, it is extremely important to elucidate how in vivo statin treatment affects immune system function.. To define the mechanisms underlying the immunomodulatory activity of lovastatin, we used a C. albicans-induced DTH model in mice, which recapitulates the coordinated cell interactions that take place during Th1 immune reactions. In our system, lovastatin attenuated the acute inflammatory response triggered by C. albicans challenge. Concurring with studies in animal models of Th1-mediated autoimmune diseases (6, 9, 15), we found that lovastatin treatment triggered a decrease in production of proinflammatory cytokines and promoted a Th2-biased DTH response. We also detected a slight reduction in MHCII expression in CD11c+ cells in lovastatin-treated mice (Fig. 6⇑A). This decrease appears not to affect ...
Our previous studies have demonstrated that epidermal growth factor (EGF) can induce cell migration through the induction of cysteine-rich protein 61 (Cyr61) in human anaplastic thyroid cancer (ATC) cells. The aim of the present study was to determine the inhibitory effects of combined treatment with the peroxisome proliferator-activated receptor-γ (PPARγ) ligand troglitazone and the cholesterol-lowering drug lovastatin at clinically achievable concentrations on ATC cell migration. Combined treatment with 5 μM troglitazone and 1 μM lovastatin exhibited no cytotoxicity but significantly inhibited EGF-induced migration, as determined using wound healing and Boyden chamber assays. Cotreatment with troglitazone and lovastatin altered the epithelial-to-mesenchymal-transition (EMT) -related marker gene expression of the cells; specifically, E-cadherin expression increased and vimentin expression decreased. In addition, cotreatment reduced the number of filopodia, which are believed to be involved in
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 ...
Orally administered drugs may be metabolized by intestinal microbial enzymes before absorption into the blood. Accordingly, coadministration of drugs affecting the metabolic activities of gut microbes (e.g., antibiotics) may lead to drug-drug interactions (DDI). In this study, gut microbiota-mediated DDI were investigated by studying the pharmacokinetics of lovastatin in antibiotic-treated rats. Incubation of lovastatin with human and rat fecalase preparations produced four metabolites, M1 (demethylbutyryl metabolite), M4 (hydroxylated metabolite), M8 (the active hydroxy acid metabolite), and M9 (hydroxylated M8), indicating involvement of the gut microbiota in lovastatin metabolism. The plasma concentration-time profiles of M8 were compared after oral administration of lovastatin to control rats or those treated with either ampicillin (100 mg/kg) or an antibiotic mixture consisting of cefadroxil (150 mg/kg), oxytetracycline (300 mg/kg), and erythromycin (300 mg/kg). Pharmacokinetic analyses ...
Lovastatin with NDC 54458-938 is a a human prescription drug product labeled by International Laboratories, Llc. The generic name of Lovastatin is lovastatin.
Lovastatin with NDC 54458-937 is a a human prescription drug product labeled by International Laboratories, Llc. The generic name of Lovastatin is lovastatin.
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
The primary cause of cardiovascular disease is atherosclerotic plaque formation. Sustained elevations of cholesterol in the blood increase the risk of cardiovascular disease. Lovastatin lowers hepatic cholesterol synthesis by competitively inhibiting HMG-CoA reductase, the enzyme that catalyzes the rate-limiting step in the cholesterol biosynthesis pathway via the mevalonic acid pathway. Decreased hepatic cholesterol levels causes increased uptake of low density lipoprotein (LDL) cholesterol and reduces cholesterol levels in the circulation. At therapeutic doses, lovastatin decreases serum LDL cholesterol by 29-32%, increases high density lipoprotein (HDL) cholesterol by 4.6-7.3%, and decrease triglyceride levels by 2-12%. HDL cholesterol is thought to confer protective effects against CV disease, whereas high LDL and triglyceride levels are associated with higher risk of disease ...
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.
LOVASTATIN- lovastatin tablet - - - Therapy with lovastatin should be a component of multiple risk factor intervention in those individuals with dyslipidemia at risk for atherosclerotic vascular disease. Lovastatin should be used in addition to a diet restricted in sa
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 - Posted in: peripheral neuropathy, lovastatin - Answer: Yes, lovastatin can cause peripheral neuropathy. Neurological: ...
Find information on Lovastatin (Altoprev, Mevacor) in Daviss Drug Guide including dosage, side effects, interactions, nursing implications, mechanism of action, half life, administration, and more. Davis Drug Guide PDF.
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.
This page on the eMedTV Web site discusses the prescription medication lovastatin extended-release, which is used to treat high cholesterol and high triglycerides. This article outlines uses, dosing, and alternatives for this medication.
Potential lovastatin side effects may be exacerbated by interactions with other prescription drugs and medications or over-the-counter products.
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 ...
1 Answer (question resolved) - Posted in: lovastatin - Answer: There is no need to wean yourself off - you can stop straight away. Why ...
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 ...
In 1997, The Life Extension Foundation published a protocol suggesting that cancer patients ask their oncologist to consider prescribing the drug lovastatin (80 mg a day) as an adjuvant therapy.
Compactin is a potent competitive inhibitor of hydroxymethylglutaryl coenzyme A reductase, the rate-limiting enzyme in cholesterol biosynthesis. Experiments were conducted with RAW264.7 cells fed 10% fetal calf serum, as per protocol PP0000002800 (pdf). Measurements were taken at 0, 12, and 24hrs for: (i) compactin, (ii) Kdo2-Lipid A, (iii) compactin + Kdo2-Lipid A. and (iv) control. ...
Visit your doctor or health care professional for regular check-ups. You may need regular tests to make sure your liver is working properly.. Tell your doctor or health care professional right away if you get any unexplained muscle pain, tenderness, or weakness, especially if you also have a fever and tiredness. Your doctor or health care professional may tell you to stop taking this medicine if you develop muscle problems. If your muscle problems do not go away after stopping this medicine, contact your health care professional.. This drug is only part of a total heart-health program. Your doctor or a dietician can suggest a low-cholesterol and low-fat diet to help. Avoid alcohol and smoking, and keep a proper exercise schedule.. Do not use this drug if you are pregnant or breast-feeding. Serious side effects to an unborn child or to an infant are possible. Talk to your doctor or pharmacist for more information.. This medicine may affect blood sugar levels. If you have diabetes, check with your ...
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. ...
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Information provided on this site is intended for use only by residents of the United States. The products discussed herein are available only upon prescription from a medical doctor or a qualified medical professional. Consumers should not construe any information herein as medical advice or as a substitute for discussions with a prescribing practitioner or other qualified medical professional. Reader understands and agrees to the foregoing. ...
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 ;. ...
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 ...
3A4V : Aids in determining therapeutic strategies for drugs that are metabolized by CYP3A4, including atorvastatin, simvastatin, and lovastatin
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
A lactone metabolite isolated from the fungus Aspergillus terreus with cholesterol-lowering and potential antineoplastic activities. Lovastatin is hydrolyzed to the active beta-hydroxyacid form, which competitively inhibits 3-hydroxyl-3-methylgutarylcoenzyme A (HMG-CoA) reductase, an enzyme involved in cholesterol biosynthesis.
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 ...
Boruta T, Bizukojc M. Culture-based and sequence-based insights into biosynthesis of secondary metabolites by Aspergillus terreus ATCC 20542. J Biotechnol. 2014 Apr 10;175:53-62. doi: 10.1016/j.jbiotec.2014.01.038. Epub 2014 Feb 15.. ...
PubMed journal article: The efficacy of intensive dietary therapy alone or combined with lovastatin in outpatients with hypercholesterolemia. Download Prime PubMed App to iPhone, iPad, or Android
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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 recent development of specific competitive inhibitors of the hydroxymethylglutaryl coenzyme A (HMG-CoA) reductase such as lovastatin, simvastatin, pravastatin and fluvastatin has provided an important new and effective approach to the treatment of hyperlipidaemia and atherosclerosis. These agent …
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 ...
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.
Cell cycle phase transitions in eukaryotic cells are driven by regulation of the activity of protein kinases known as cyclin-dependent kinases (Cdks). A broad spectrum Cdk-inhibitory activity associated with a 28-kilodalton protein (p28Ick1) was induced in cells treated with the drug lovastatin or upon density-mediated growth arrest and was periodic in the cell cycle, with peak activity in G1. The p28Ick1 protein was shown to be identical to p27Kip1, and the periodic or induced inhibitory activity resulted from a periodic accumulation of the protein. Variations in the amount of p27 protein occurred, whereas the abundance of the p27 messenger RNA remained unchanged. In every instance investigated, the posttranscriptional alteration of p27 protein levels was achieved in part by a mechanism of translational control, although in density-arrested fibroblasts and thymidine-arrested HeLa cells the half-life of the protein was also changed. ...
TY - JOUR. T1 - G1 control in mammalian cells. AU - Reed, S. I.. AU - Bailly, E.. AU - Dulic, V.. AU - Hengst, L.. AU - Resnitzky, D.. AU - Slingerland, J.. PY - 1994. Y1 - 1994. N2 - Cyclin-dependent kinases (Cdks) control the major cell cycle transitions in eukaryotic cells. On the basis of a variety of experiments where cyclin function either is impaired or enhanced, D-type cyclins as well as cyclins E and A have been linked to G1 and G1/S phase roles in mammalian cells. We therefore sought to determine if agents that block the G1/S phase transition do so at the level of regulating the Cdk activities associated with these cyclins. A variety of conditions that lead to G1 arrest were found to correlate with accumulation of G1-specific Cdk inhibitors, including treatment of fibroblasts with ionizing radiation, treatment of epithelial cells with TGF-beta, treatment of HeLa cells with the drug lovastatin, and removal of essential growth factors from a variety of different cell types. ...
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.
Mar-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.
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.
Jamp-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)...
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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
Merck & Co will have to demonstrate that its cholesterol-lowering agent, Mevacor (lovastatin), can be used safely without a prescription in order to win US Food and Drug Administration clearance as an over-the-counter product, an FDA advisory committee revealed yesterday. - News - PharmaTimes
Cholesterol-lowering statin drugs may also reduce the risk of developing rheumatoid arthritis by over 40%, the Daily Mail reported. The news is based on a la...
... (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" ...
... lovastatin, and simvastatin, but other studies have not found a connection.[81] Lovastatin induces the expression of gene ... Lovastatin + niacin extended-release. Advicor, Mevacor. Combination therapy. Atorvastatin + amlodipine. Caduet, Envacar. ... Lovastatin, a compound isolated from Aspergillus terreus, was the first statin to be marketed. ... By 1978, Merck had isolated lovastatin (mevinolin, MK803) from the fungus Aspergillus terreus, first marketed in 1987 as ...
Lovastatin, the first 'statin' drug, was first marketed in 1987. In animal models and in vitro, niacin produces marked anti- ... Extended release niacin was combined with the lovastatin trade-named Advicor, and with simvastatin, trade-named Simcor as ... "Advicor (Niacin Extended-Release & Lovastatin) Tablets". U.S. Food and Drug Administration; Drug Approval Package. 13 September ...
LOVASTATIN 298. LOXAPINE 299. MEBENDAZOLE 300. MEBEVERINE HYDROCHLORIDE 301. MEDROXY PROGESTERONE ACETATE ...
If products do not contain lovastatin, do not claim to contain lovastatin, and do not make a claim to lower cholesterol, they ... Lovastatin became the patented, prescription drug Mevacor. Red yeast rice went on to become a non-prescription dietary ... Lovastatin became the patented, prescription drug Mevacor. Red yeast rice went on to become a non-prescription dietary ... Lovastatin and other prescription statin drugs inhibit cholesterol synthesis by blocking action of the enzyme HMG-CoA reductase ...
Lovastatin occurs naturally in low concentrations in oyster mushrooms, red yeast rice, and Pu-erh. Lovastatin's mode of action ... Zhao ZJ, Pan YZ, Liu QJ, Li XH (June 2013). "Exposure assessment of lovastatin in Pu-erh tea". International Journal of Food ... Lovastatin was the first FDA approved secondary metabolite to lower cholesterol levels. ... Erythromycin Lovastatin and other statins Discodermolide Aflatoxin B1 Avermectins Nystatin Rifamycin Fatty acid synthase ...
Examples of statins include atorvastatin, lovastatin, rosuvastatin, and simvastatin. They are used in the treatment of ...
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 ...
Besides that, there were findings that lovastatin induce CYP4F2. There also have been findings that CYP4F2 is inhibited by ... "Regulation of human cytochrome P450 4F2 expression by sterol regulatory element-binding protein and lovastatin". The Journal of ...
Concomitant use with cholesterol medications such as lovastatin or simvastatin. Hypersensitivity to clarithromycin or any ...
In Canada, this also applies to bosentan, lovastatin and rosuvastatin; and in the EU, to dabigatran, atorvastatin, and ...
It has been reported to produce sterigmatocystin, citrinin, and lovastatin. A. flavipes has been cultivated on both Czapek ...
Holstein SA, Hohl RJ (2003). "Synergistic interaction of lovastatin and paclitaxel in human cancer cells". Mol. Cancer Ther. 1 ...
Lovastatin is typically produced within fermentation conditions of the fungus. Fast growth of filamentous hyphae in the species ... It is also used to produce the drug simvastatin that is chemically related to lovastatin and used to lower cholesterol. Thom C ... doi:10.1016/s0141-0229(03)00130-3. Szakacs, G; Morovjan G.; Tengerdy R (1998). "Production of lovastatin by a wild strain of ... It was also the initial source for the drug mevinolin (lovastatin), a drug for lowering serum cholesterol. Aspergillus terreus ...
"Brochure: The History of Drug Regulation in the United States". Tobert, Jonathan A. (July 2003). "Lovastatin and beyond: the ... By 1978, Merck had isolated lovastatin (mevinolin, MK803) from the fungus Aspergillus terreus, first marketed in 1987 as ...
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 ...
Tobert JA (July 2003). "Lovastatin and beyond: the history of the HMG-CoA reductase inhibitors". Nature Reviews. Drug Discovery ... lovastatin, fluvastatin and pravastatin". Clinical Pharmacokinetics. 47 (7): 463-74. doi:10.2165/00003088-200847070-00003. PMID ...
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. ...
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 ...
Werner B, Dittmann S, Funke C, Überla K, Piper C, Niehaus K, Horstkotte D, Farr M (Apr 2014). "Effect of lovastatin on ...
Lovastatin, the first commercial statin, was extracted from a fermentation broth of Aspergillus terreus. Industrial production ... Jahromi MF, Liang JB, Ho YW, Mohamad R, Goh YM, Shokryazdan P (2012). "Lovastatin production by Aspergillus terreus using agro- ... Tobert JA (July 2003). "Lovastatin and beyond: the history of the HMG-CoA reductase inhibitors". Nature Reviews. Drug Discovery ... The red yeast rice fungus, Monascus purpureus, can synthesize lovastatin, mevastatin, and the simvastatin precursor monacolin J ...
August 31 - The FDA for the first time approves a statin, lovastatin. September 5 - The first successful surgical separation of ...
The statins lovastatin, mevastatin, and simvastatin precursor monacolin J, are fungal isolates. Additional fungal isolates that ...
Campbell, Chantel D.; Vederas, John C. (23 June 2010). "Biosynthesis of lovastatin and related metabolites formed by fungal ... as a side chain of lovastatin formed by its diketide synthase (LovF) during its biosynthesis-this result constitutes the first ...
Some examples of secondary metabolites are penicillin, cyclosporin A, gibberellin, and lovastatin. Primary metabolites are ...
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- ...
Merck scientists also developed lovastatin, the first drug of the statin class. It was marketed under the trade name Mevacor. ...
Lovastatin (also known as mevinolin) is produced by Aspergillus terreus Gent, Janneane F; Ren, Ping; Belanger, Kathleen; Triche ... Several statin cholesterol-lowering drugs (such as lovastatin, from Aspergillus terreus) are derived from molds. The ...
Soon after, lovastatin, the first commercial statin, was found in the Aspergillus mold. Although mevastatin never became an ...
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" ...
Lovastatin: learn about side effects, dosage, special precautions, and more on MedlinePlus ... If you become pregnant while taking lovastatin, stop taking lovastatin and call your doctor immediately. Lovastatin may harm ... Before taking lovastatin,. *tell your doctor and pharmacist if you are allergic to lovastatin, any other medications, or any of ... Continue to take lovastatin even if you feel well. Do not stop taking lovastatin without talking to your doctor. ...
... 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 ...
... lovastatin - Answer: Yes, lovastatin can cause peripheral neuropathy. Neurological: ... ... Home › Q & A › Questions › Can Lovastatin cause.... Can Lovastatin cause neuropathy?. Asked. 11 Jan 2012 by mike8. Active. 13 ... Side Effects of Lovastatin (detailed). Search for questions. Still looking for answers? Try searching for what you seek or ask ... Yes, lovastatin can cause peripheral neuropathy.. Neurological: dysfunction of certain cranial nerves (including alteration of ...
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 ...
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 b.i.d ... Lovastatin acid refers to the β-hydroxyacid of lovastatin.. ‡ The mean total AUC of lovastatin without itraconazole phase could ... Lovastatin significantly decreased plasma total-C, LDL-C, total-C/HDL-C ratio and LDL-C/HDL-C ratio. In addition, lovastatin ... The effect of lovastatin on lipids and lipoproteins and the safety profile of lovastatin were similar to that demonstrated in ...
Prescriber Checkup » LOVASTATIN LOVASTATIN. Mevacor (Lovastatin) is cholesterol-lowering medicine called a statin. It lowers ... Top prescribers for LOVASTATIN. « First ‹ Prev 1 2 3 4 5 6 7 … Next › Last » ...
Lovastatin. A fungal metabolite isolated from cultures of Aspergillus terreus. The compound is a potent anticholesteremic agent ... All MeSH CategoriesChemicals and Drugs CategoryPolycyclic CompoundsPolycyclic Aromatic HydrocarbonsNaphthalenesLovastatin ... AromaticPolycyclic Aromatic HydrocarbonsNaphthalenesLovastatinSimvastatinEzetimibe, Simvastatin Drug Combination ...
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 ...
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 ...
... Am J Cardiol. 2002 Jun 15;89(12):1374-80. doi: 10.1016/s0002-9149(02)02355-x. ... With lovastatin, the rate is approximately 1/1.14 million patient-treatment years, which is 9% of the background rate of all ... The first of the statins, lovastatin, was approved in 1986 and has acquired 24 million patient-years of clinical experience. ... of patients on lovastatin doses of 20 and 80 mg/day, respectively. These elevations are reversible with continuing therapy, are ...
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 ...
WebMD provides information about interactions between Lovastatin Oral and atorvastatin-40mg-lovastatin-simvastatin- ... Drugs & MedicationsLovastatin. Atorvastatin (, 40mg): Lovastatin; Simvastatin/Ciprofloxacin Interactions. This information is ...
The lovastatin-synthesizing enzyme is one of the most interesting but least understood of the polyketide synthases, which are ... Tangs team has been able to recapture all of the steps needed to make the lovastatin precursor molecule. And with this, Tang ... "In this study, we studied the enzyme that makes a small-molecule precursor to lovastatin. And whats really different about ... UCLA Researchers Reconstitute Enzyme That Synthesizes Cholesterol Drug Lovastatin. by Sam Savage ...
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 ...
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 ...
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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Lovastatin is hydrolyzed to the active beta-hydroxyacid form, which competitively inhibits 3-hydroxyl-3-methylgutarylcoenzyme A ... Lovastatin Sodium. Mevinolin. Monacolin K. US brand name:. Mevacor. Chemical structure:. (2S)-2-methylbutanoic acid, (1S,3R,7S, ... lovastatin A lactone metabolite isolated from the fungus Aspergillus terreus with cholesterol-lowering and potential ... Lovastatin is hydrolyzed to the active beta-hydroxyacid form, which competitively inhibits 3-hydroxyl-3-methylgutarylcoenzyme A ...
Some side effects may occur that usually do not need medical attention. These side effects may go away during treatment as your body adjusts to the medicine. Also, your health care professional may be able to tell you about ways to prevent or reduce some of these side effects. Check with your health care professional if any of the following side effects continue or are bothersome or if you have any questions about them:. ...
Drug: Lovastatin Lovastatin 40 mg daily (2 tablets of 20 mg each, p.o.), during twelve months until the end of the study, or ... Lovastatin: Immunomodulatory Value Evaluation (LIVE). The safety and scientific validity of this study is the responsibility of ... In this arm, subjects will receive 40 mg of Lovastatin (2 tablets of 20 mg each, p.o.), in a daily doses, during twelve months ... Mazière JC, Landureau JC, Giral P, Auclair M, Fall L, Lachgar A, Achour A, Zagury D. Lovastatin inhibits HIV-1 expression in H9 ...
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 ...
Acute and subacute hepatotoxicities were analyzed with or without lovastatin co-treatment. Lovastatin protected the liver ... Ceramide production, however, was not blocked by lovastatin, indicating that hepatoprotection by lovastatin is independent of ... Hepatoprotection by lovastatin was due to a reduced induction of DNA damage following doxorubicin treatment. The statin also ... The lipid lowering drug lovastatin protects against doxorubicin-induced hepatotoxicity.. Henninger C1, Huelsenbeck J, ...
Tissue selectivity of pravastatin sodium, lovastatin and simvastatin - The relationship between inhibition of de novo sterol ...
Lovastatin is in a group of drugs called HMG CoA reductase inhibitors, or... ... Lovastatin and niacin is usually taken at bedtime with a low-fat snack. Do not take lovastatin and niacin on an empty stomach. ... Lovastatin is in a group of drugs called HMG CoA reductase inhibitors, or "statins." Lovastatin reduces levels of "bad" ... Do not take lovastatin and niacin if you are pregnant.Stop taking this medication and tell your doctor right away if you become ...
When added in vitro to cell incubations, lovastatin stimulated de novo fatty acid synthesis and acetyl-CoA carboxylase activity ... The in vitro and in vivo effects of lovastatin on fatty acid metabolism were studied in isolated rat hepatocytes. ... Lovastatin depressed palmitate, but not octanoate, oxidation. This may be attributed to the lovastatin-induced increase in ... Effects of lovastatin on hepatic fatty acid metabolism Lipids. 1993 Dec;28(12):1087-93. doi: 10.1007/BF02537075. ...
... is potent inhibitor of 3-hydroxy-3-methylglutaryl-coenzyme A reductase (HMG-CoA reductase) that was initially ...
MayoClinic.com: Lovastatin Side Effects * Los Angeles Times; Pinning Down the Side Effects of Statins; Devon Schuyler; Aug. 9 ... Certain people are at higher risk for developing side effects when taking lovastatin, simvastatin or pravastatin. Having to ... Three popular examples of statins are lovastatin, simvastatin and pravastatin; these medications have some side effects in ...
Lovastatin belongs to the family of medications known as lipid metabolism regulators. It is used in addition to diet and ... Do not take lovastatin if you: *are allergic to lovastatin or any ingredients of the medication ... Lovastatin belongs to the family of medications known as lipid metabolism regulators. It is used in addition to diet and ... Diabetes: Lovastatin may cause an increase in blood sugar levels (may cause a loss of blood glucose control) and glucose ...
In the present study, the effect of lovastatin, an inhi ... The effect of lovastatin on cell growth was irreversible after ... Mevalonic acid (1 mmol/L) reversed lovastatin-induced inhibition of cell growth if it was added with lovastatin (2.5 micrograms ... Lovastatin / antagonists & inhibitors, pharmacology*. Mevalonic Acid / pharmacology. Mice. Mice, Nude. Pancreatic Neoplasms / ... Inhibition of cell growth was observed with lovastatin doses at or above 2.5 micrograms/mL for H2T, CAV, MIA Paca2, and CAPAN2 ...
  • Niacin/lovastatin (trade names Advicor , Mevacor ) is a drug combination used for the treatment of dyslipidemia . (wikipedia.org)
  • Mevacor (Lovastatin) is cholesterol-lowering medicine called a statin. (propublica.org)
  • Lovastatin , sold under the brand name Mevacor among others, is a statin medication , to treat high blood cholesterol and reduce the risk of cardiovascular disease . (wikipedia.org)
  • Do not take Mevacor or Altoprev if you are allergic to lovastatin or any ingredients contained in this drug. (rxlist.com)
  • You should not take this medication if you are allergic to niacin (Niaspan, Niacor, and others) or lovastatin (Altoprev, Mevacor), if you are pregnant or breast-feeding, or if you have liver disease, severe bleeding, or a stomach ulcer. (cardiosmart.org)
  • Lovastatin, marketed under the name Mevacor and Altocor (no longer available) and Altoprev, is one of a class of prescription medications called statins. (herbal-supplements-guide.com)
  • FDA testing revealed the products contain lovastatin, the active ingredient in Mevacor, a prescription drug approved for marketing in the United States as a treatment for high cholesterol. (ronpaulforums.com)
  • Lovastatin (Mevacor), marketed by Merck under the brand name 'Mevacor', was the first statin class medication ever to come out on the market in the 1980's. (cholesterolcholestrol.com)
  • Lovastatin (Mevacor) is also one of the less potent of the statin class of medications, but it's widely taken and generally well tolerated. (cholesterolcholestrol.com)
  • Keep in mind these are the highest percentages found, and will not necessarily reflect your progression or your level of benefit from taking Lovastatin (Mevacor). (cholesterolcholestrol.com)
  • One of the nice things about lovastatin (Mevacor) is that it's the oldest statin medication, which means doctors and scientists have had plenty of time to study it since the 1970's when it was first found. (cholesterolcholestrol.com)
  • While lovastatin (Mevacor) is thought of as reasonably safe, completely safe is not part of the description of any prescription medication. (cholesterolcholestrol.com)
  • As with all medications, bigger doses of Lovastatin (Mevacor) are not always better. (cholesterolcholestrol.com)
  • Pregnant or nursing mothers should never take lovastatin (Mevacor) unless the benefit to the mother clearly justifies the risk to the unborn child. (cholesterolcholestrol.com)
  • The guidelines published by Merck state that you'll want to get a blood analysis of liver function before starting or raising the daily dose of lovastatin (Mevacor) just to check for initial unexplained high liver enzymes, as well as 12 weeks after both starting and increasing the daily dosage. (cholesterolcholestrol.com)
  • If liver problems are going to develop because of Lovastatin (Mevacor), they generally tend to do so within the first three to twelve months, so ongoing careful checking during that first year is a good idea. (cholesterolcholestrol.com)
  • However, unlike rosuvastatin (Crestor), simvastatin (Zocor) and pravastatin (Pravachol), lovastatin (Mevacor) is generally considered safe to take for people with kidney damage as long as a doctor keeps a close eye on it. (cholesterolcholestrol.com)
  • Lovastatin (Mevacor) has been tested on children, and has proven relatively safe at a maximum dose of 40 mg per day for boys past puberty and girls who have been menstruating for at least a year down to 10 years of age. (cholesterolcholestrol.com)
  • Generic for Mevacor (Lovastatin) is a cholesterol-lowering medication that helps prevent heart attacks and strokes. (internationaldrugmart.com)
  • Lovastatin (Mevacor) is a prescription medication used for treating a number of conditions related to heart disease, including high cholesterol. (rateadrug.com)
  • Lovastatin (Mevacor) is a medication that has been licensed to treat several conditions. (rateadrug.com)
  • Lovastatin (Mevacor) may interact with a number of other medications. (rateadrug.com)
  • Some of these drug interactions with lovastatin may increase your risk for developing serious muscle problems (see Mevacor and Muscle Pain). (rateadrug.com)
  • Statin drugs such as lovastatin (Mevacor) inhibit the enzyme known as 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase. (dynamicchiropractic.com)
  • Lovastatin is sold under the brand-name Mevacor by Merck & Co. It is Pregnancy Category X, which means studies in humans or animals have linked it to an increased risk of birth defects and these risks outweigh any benefit for the mother. (schmidtlaw.com)
  • 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)
  • In the present study, the effect of lovastatin, an inhibitor of 3-hydroxy-3-methylglutaryl coenzyme A, the rate-limiting enzyme of cholesterol synthesis, on the growth of five pancreatic cancer cell lines (human-CAV, MIA Paca2, CAPAN2 and PANC1, and hamster-H2T) in vitro and of two cell lines (CAV and H2T) in vivo was examined. (biomedsearch.com)
  • The effect of lovastatin on cell growth was irreversible after 48 hours of exposure. (biomedsearch.com)
  • BACKGROUND AND OBJECTIVES: This study was performed to investigate the antiproliferative effect of lovastatin on vascular smooth muscle cell, especially to determine whether lovastatin induces apoptosis in vascular smooth muscle cell and the products of mevalonate pathway can reverse the antiproliferative effect of lovastatin. (koreamed.org)
  • The antiproliferative effect of lovastatin may result from the induction of apoptosis in vascular smooth muscle cells. (koreamed.org)
  • The effect of lovastatin on efferocytosis was investigated in primary human macrophages, in the murine lung, and in human alveolar macrophages taken from patients with chronic obstructive pulmonary disease. (jimmunol.org)
  • This project aims to test the safety and synergistic effect of lovastatin and minocycline combined treatment in patients with Fragile X syndrome. (fraxa.org)
  • Lovastatin Where Buy In Safely Online plus Order Lovastatin 20Mg. (lanyrd.com)
  • I was told to take LOVASTATIN 20MG TABLETS to protect me. (medications.com)
  • In addition, Annexin V apoptotic studies revealed that lovastatin enhances paclitaxel-induced apoptosis in HL-60 cells. (aacrjournals.org)
  • Because of the increased sensitivity of neuroblastoma cells to lovastatin-induced apoptosis, we examined the effect of this agent on a variety of tumor cells, including leukemic cell lines and primary patient samples. (bloodjournal.org)
  • Based on a variety of cytotoxicity and apoptosis assays, the 6 acute lymphocytic leukemia cell lines tested displayed a weak apoptotic response to lovastatin. (bloodjournal.org)
  • In contrast, the majority of the acute myeloid leukemic cell lines (6/7) and primary cell cultures (13/22) showed significant sensitivity to lovastatin-induced apoptosis, similar to the neuroblastoma cell response. (bloodjournal.org)
  • 1 5 Prolonged exposure of various tumor-derived cell lines to relatively high concentrations of lovastatin (30 to 100 μmol/L) can lead to cellular apoptosis. (bloodjournal.org)
  • 3)Lovastatin-treated vascular smooth muscle cells showed typical morphological changes of apoptosis. (koreamed.org)
  • 1308-1318, 1999) that lovastatin, a prototypic member of the statin family, can induce apoptosis of human acute myeloid leukemia (AML) cells in a sensitive and specific manner. (aacrjournals.org)
  • This suggests protein geranylgeranylation is an essential downstream component of the mevalonate pathway for cerivastatin similar to lovastatin-induced apoptosis. (aacrjournals.org)
  • We have reported previously (3) that one member of the statin family, lovastatin, triggers apoptosis in established and primary AML cells but not in normal bone marrow progenitors at doses that are achievable in vivo . (aacrjournals.org)
  • Apoptosis was induced using the hydroxymethyl glutaryl CoA reductase inhibitor, lovastatin, and was evaluated by agarose gel electrophoresis of genomic DNA, morphological criteria, and terminal deoxynucleotidyl transferase-mediated nick end labeling. (aacrjournals.org)
  • Lovastatin (30 µ m ) was an effective inducer of apoptosis, causing changes that were evident after 48 h and essentially complete after 96-120 h of treatment. (aacrjournals.org)
  • Caspase-7, but not caspase-3, underwent proteolytic activation during lovastatin-induced apoptosis, an effect prevented by mevalonate. (aacrjournals.org)
  • Lovastatin-induced apoptosis also was prevented when the caspase inhibitors Z-DEVD-CH 2 F or Z-VAD-CH 2 F (100 µ M ) where added to the medium. (aacrjournals.org)
  • These studies have identified lovastatin as a powerful inducer of apoptosis in the cell line LNCaP. (aacrjournals.org)
  • Caspase activation was a necessary event for LNCaP cells to undergo apoptosis during treatment with lovastatin. (aacrjournals.org)
  • Identification of caspase-7 as a potential mediator of lovastatin-induced apoptosis broadens our knowledge of the molecular events associated with programmed cell death in a cell line derived from prostatic epithelium. (aacrjournals.org)
  • We have now extended this work and evaluated a wide variety and large number of tumor-derived cell lines for their sensitivity to lovastatin-induced apoptosis. (aacrjournals.org)
  • These cell lines were exposed to a wide range (0-100μ m ) of lovastatin for 2 days and assayed for cell viability using the 3,4,5-dimethyl thiazlyl-2,2,5-diphenyltetrazolium bromide assay and the induction of apoptosis by flow cytometric and ultrastructural analyses. (aacrjournals.org)
  • Interestingly, the subset of malignancies that are particularly sensitive to lovastatin-induced apoptosis correspond to those tumor subtypes that are sensitive to the biological and antiproliferative effects of retinoids in vitro . (aacrjournals.org)
  • Thus, we have identified a subset of tumors that are sensitive to lovastatin-induced apoptosis and show HMG-CoA reductase as a potential therapeutic target of these cancers. (aacrjournals.org)
  • Consistent with initiation of apoptosis, cellular caspase-8, caspase-9 and caspase-3 activities were elevated in lovastatin-treated cells. (oup.com)
  • Since immunoelectron microscopy showed translocation of Bax to the mitochondria in lovastatin-treated cells, lovastatin-induced apoptosis may, therefore, be ultimately dependent on Bax induction of cytochrome c release. (oup.com)
  • These results suggest that lovastatin may be useful as an adjuvant therapy in breast cancers containing p53 mutations due to its ability to both suppress DNA synthesis and induce p53-independent mitochondria-mediated apoptosis. (oup.com)
  • Cell-cycle gene expression in lovastatin-induced medulloblastoma apoptosis. (mysciencework.com)
  • Lovastatin-induced growth inhibition and apoptosis in medulloblastoma are not dependent on the regulation of Ras and c-myc gene expression, but may be mediated by p27KIP1 gene expression. (mysciencework.com)
  • Lovastatin-induced apoptosis in medulloblastoma is probably p53 independent, but p53 and p21WAF1 gene expression may also mediate anti-proliferative effects of lovastatin on specific medulloblastoma cell lines. (mysciencework.com)
  • Tissue selectivity of pravastatin sodium, lovastatin and simvasta. (ingentaconnect.com)
  • Certain people are at higher risk for developing side effects when taking lovastatin, simvastatin or pravastatin. (livestrong.com)
  • We show that while the lovastatin open-ring form and pravastatin (a lovastatin analogue, 100% open ring) inhibit the HMG-CoA reductase enzyme, lovastatin pro-drug inhibits the proteasome but does not inhibit HMG-CoA reductase. (pnas.org)
  • Lovastatin is a cholesterol lowering agent, along with its family member's simvastatin, atorvastatin and pravastatin [ 10 ]. (alliedacademies.org)
  • Lovastatin tablets are supplied as 10 mg, 20 mg and 40 mg tablets for oral administration. (nih.gov)
  • Do not break, chew, or crush the lovastatin extended-release tablets. (emedtv.com)
  • As with atorvastatin , simvastatin , and other statin drugs metabolized via CYP3A4 , drinking grapefruit juice during lovastatin therapy may increase the risk of side effects. (wikipedia.org)
  • In this study, we compare the potency of the synthetic statins (fluvastatin, atorvastatin, and cerivastatin) to lovastatin (Fig. 1) ⇓ for their ability to inhibit AML cell viability. (aacrjournals.org)
  • Lovastatin is one of the prototypic inhibitors of HMG-CoA reductase and is derived from fungal fermentation, whereas atorvastatin, cerivastatin, and fluvastatin are newer synthetic inhibitors of this rate-limiting enzyme of the mevalonate pathway. (aacrjournals.org)
  • particularly if taking with prescription "statins" such as lovastatin, simvastatin, or atorvastatin. (schmidtlaw.com)
  • Comparison of one-year efficacy and safety of atorvastatin versus lovastatin in primary hypercholesterolemia. (semanticscholar.org)
  • Take lovastatin at around the same time(s) every day. (medlineplus.gov)
  • Take lovastatin exactly as directed. (medlineplus.gov)
  • [11] Patients with liver disease should not take lovastatin. (wikipedia.org)
  • If you also take certain other drugs to lower your cholesterol (bile acid-binding resins such as cholestyramine or colestipol ), take lovastatin at least 1 hour before or at least 4 hours after taking these medications. (webmd.com)
  • In addition, people with active liver disease or unexplained high levels of liver enzymes in their blood should also not take lovastatin. (cholesterolcholestrol.com)
  • You should not take lovastatin if you have active liver disease, or if you are pregnant or breastfeeding. (uncmedicalcenter.org)
  • You should not take lovastatin if you are allergic to it, if you are pregnant or breast-feeding, or if you have active liver disease. (unclenoir.org)
  • Lovastatin is in a class of medications called HMG CoA reductase inhibitors (statins). (medlineplus.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)
  • Lovastatin is in a group of drugs called HMG CoA reductase inhibitors, or "statins. (cardiosmart.org)
  • Previously, we reported that lovastatin can be used to arrest cultured cells in the G 1 phase of the cell cycle, resulting in the stabilization of the cyclin-dependent kinase inhibitors (CKIs) p21 and p27. (pnas.org)
  • The cytotoxicity of lovastatin is evidenced in that lovastatin can induce cell cycle arrest in vitro in both G 1 and G 2 -M. The G 1 effect has been the most closely examined and is associated with lovastatin-induced decreases in cyclin A, D, and E levels ( 9 ) and increases in cyclin-dependent kinase inhibitors ( 10 ). (aacrjournals.org)
  • Lovastatin belongs to a group of drugs called HMG-CoA reductase inhibitors, also known as statins. (rxwiki.com)
  • To determine whether lovastatin, HMG-CoA-reductase inhibitors, influences TGF-β-induced myofibroblast transdifferentiation in porcine lens epithelial cells (LECs). (arvojournals.org)
  • Lovastatin, also called Monacolin K, a natural product derived from Monascus or Aspergillus -fermented rice, is a member of the statin class of drugs known as 3-hydroxy-3-methyl-glutaryl-CoA (HMG-CoA) reductase inhibitors. (jcancer.org)
  • Lovastatin has severe/serious/moderate/mild interactions with at least 34 different drugs. (rxlist.com)
  • Drug interactions are reported among people who take Ritalin and Lovastatin together. (ehealthme.com)
  • Lovastatin is clinically used to treat patients with hypercholesterolemia and successfully lowers cholesterol levels. (pnas.org)
  • Lovastatin is used for the treatment of hypercholesterolemia ( 11 ) because it inhibits hydroxymethyl-glutaryl (HMG)-CoA reductase, and thus prevents HMG-CoA's conversion into mevalonic acid ( 12 , 13 ). (pnas.org)
  • The hydroxymethylglutaryl-CoA reductase inhibitor lovastatin is used widely to treat hypercholesterolemia and has been shown to have cell cycle-specific effects. (aacrjournals.org)
  • Lovastatin, a hydroxymethylglutaryl-CoA reductase inhibitor, has traditionally been used to treat hypercholesterolemia ( 1 , 2 ). (aacrjournals.org)
  • The HMG-CoA reductase inhibitor, lovastatin, which is used extensively in the treatment of hypercholesterolemia, induced a potent apoptotic response in human neuroblastoma cells. (bloodjournal.org)
  • Lovastatin is a specific, nonreversible competitive inhibitor of HMG-CoA reductase, whose ability to block this critical metabolic pathway has led to its extensive clinical use as a treatment for hypercholesterolemia. (bloodjournal.org)
  • 8 The therapeutic dose for treatment of hypercholesterolemia is approximately a 1 mg/kg/d oral dose that produces serum levels in the order of 0.1 μmol/L lovastatin. (bloodjournal.org)
  • One hundred eleven outpatients with moderate hypercholesterolemia were treated at five lipid clinics with the National Cholesterol Education Program Step 2 diet (which is low in fat and cholesterol) and lovastatin (20 mg once daily), both alone and together. (unboundmedicine.com)
  • Homozygous Familial Hypercholesterolemia: Use of lovastatin for this rare genetic disorder (increased cholesterol levels) is not sufficient enough for treatment. (rxwiki.com)
  • Inhibition of this enzyme could also inhibit the intrinsic biosynthesis of coenzyme Q10 (CoQ10), but there have not been definitive data on whether lovastatin reduces levels of CoQ10 as it does cholesterol. (pnas.org)
  • We have conducted three related protocols to determine whether lovastatin does indeed inhibit the biosynthesis of CoQ10. (pnas.org)
  • Components of grapefruit juice, the flavonoid naringin , or the furanocoumarin bergamottin inhibit CYP3A4 in vitro , [13] and may account for the in vivo effect of grapefruit juice concentrate decreasing the metabolic clearance of lovastatin, and increasing its plasma concentrations. (wikipedia.org)
  • buy lovastatin next day cod For those that are truly concerned about improving their health, Most of the known NSAIDs inhibit primarily COX- purchase lovastatin florida lovastatin backorder 2016 uk purchase lovastatin Hobart lovastatin generic buy on line uk order female lovastatin online can i buy lovastatin pharmacy can you order lovastatin online in canada T3 and T4 are both important in a person's metabolism. (lanyrd.com)
  • In this report we show that this stabilization of p21 and p27 may be the result of a previously unknown function of the pro-drug, β-lactone ring form of lovastatin to inhibit the proteasome degradation of these CKIs. (pnas.org)
  • These findings suggest that the pro-drug form of another β-lactone, lovastatin, similar in structure to lactacystin, may inhibit the ubiquitin-mediated proteolysis of key regulatory proteins such as the cyclins and CKIs. (pnas.org)
  • The hydroxymethylglutaryl-coenzyme A reductase inhibitor lovastatin is known to inhibit cell cycle progression. (asnjournals.org)
  • The nature of the biologically active form of lovastatin has been challenged recently as the growth-inhibitory effects of this drug were attributed to its prodrug lactone form that does not inhibit HMG-CoA reductase function. (aacrjournals.org)
  • Among the CV drugs screened, simvastatin and lovastatin were shown to inhibit the liver metabolism of sinomenine with Ki values of 13.00 and 25.83 μM, respectively. (ovid.com)
  • Lovastatin is shown to inhibit the cell proliferation, cell migration, and cell adhesion of cancer cells [ 11 ]. (alliedacademies.org)
  • The expressions of Runx2 and collagen I by immunofluorescence decreased as the dose of lovastatin increased. (alliedacademies.org)
  • The high dose of lovastatin also inhibited lung metastasis. (oup.com)
  • When mevalonate levels decrease as a response to lovastatin, isoprenylation of key signal transduction proteins (e.g. (pnas.org)
  • It will also seek to establish correlations between platelets biomarkers and clinical response to lovastatin and/or minocycline. (fraxa.org)
  • These results indicate that mevalonic acid or a metabolite in the cholesterol synthesis pathway is necessary for growth of pancreatic cancer cells and suggest that lovastatin should be further examined as a potential therapeutic agent for pancreatic cancer. (biomedsearch.com)
  • Our findings therefore suggest that lovastatin hinders the delivery of intracellular cholesterol to the plasma membrane, resulting in increased free cholesterol and lower levels of cholesteryl ester in cholesterol-loaded cells. (ahajournals.org)
  • Administration of lovastatin to cells in culture impacts cell cycle progression. (pnas.org)
  • The plasma concentration-time profiles of M8 were compared after oral administration of lovastatin to control rats or those treated with either ampicillin (100 mg/kg) or an antibiotic mixture consisting of cefadroxil (150 mg/kg), oxytetracycline (300 mg/kg), and erythromycin (300 mg/kg). (aspetjournals.org)
  • 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)
  • Although a successful drug, lovastatin does have side effects, particularly including liver dysfunction, which presumably can be caused by the lovastatin-induced deficiency of CoQ10. (pnas.org)
  • Lovastatin protected the liver against doxorubicin-induced acute pro-inflammatory and pro-fibrotic stress responses as indicated by an attenuated mRNA expression of tumor necrosis factor alpha (TNFα) and connective tissue growth factor (CTGF), respectively. (nih.gov)
  • Before taking lovastatin and niacin, tell your doctor if you have ever had liver or kidney disease, heart disease, diabetes, gout, or a thyroid disorder, if you have recently had a heart attack, or if you drink more than 2 alcoholic beverages daily. (cardiosmart.org)
  • Lovastatin undergoes extensive first-pass extraction in the liver, its primary site of action, with subsequent excretion of drug equivalents in the bile. (nextbio.com)
  • The Lovastatin prescription information also warns: "The drug should be used with caution in patients who consume substantial quantities of alcohol and/or have a past history of liver disease . (herbal-supplements-guide.com)
  • ALT 3 x the upper limit of normal (ULN) occur in 2.6% and 5.0% of patients on lovastatin doses of 20 and 80 mg/day, respectively. (nih.gov)
  • Inhibition of cell growth was observed with lovastatin doses at or above 2.5 micrograms/mL for H2T, CAV, MIA Paca2, and CAPAN2 or 10 micrograms/mL in PANC1. (biomedsearch.com)
  • The survival fraction of H2T cells was markedly decreased by 1- or 24-hour exposure to 75 micrograms/mL but not to doses ranging from 0.5 to 60 micrograms/mL of lovastatin. (biomedsearch.com)
  • however, at these doses, the achievable peak serum levels of lovastatin were only in the range of 0.1 to 3.92 μmol/L and, as such, had little effect in reducing tumor load. (bloodjournal.org)
  • The effects of lovastatin extended-release on cholesterol and triglyceride levels were generally even greater for the higher doses. (emedtv.com)
  • Results MCF 7 cells treated with different doses of lovastatin for 48~72 h had no significant effect on the protein level of ERK1, but the activities of ERK1 and the P38 MAPK proteins were down regulated at 72 h after treatment. (cnki.com.cn)
  • Lovastatin is hydrolyzed to the active beta-hydroxyacid form, which competitively inhibits 3-hydroxyl-3-methylgutarylcoenzyme A (HMG-CoA) reductase, an enzyme involved in cholesterol biosynthesis. (cancer.gov)
  • Lovastatin inhibits mesangial cell proliferation via p27Kip1. (asnjournals.org)
  • Lovastatin inhibits TGF-β-induced myofioblast transdifferentiation of cultured porcine LECs. (arvojournals.org)
  • In the present study, we employed a novel antibody microarray technology to investigate the molecular mechanisms through which lovastatin inhibits breast cancer. (jcancer.org)
  • Lovastatin inhibits tu. (oup.com)
  • 3 5-7 The growth arrest and apoptotic properties of lovastatin has led to its evaluation as a potential therapeutic agent in the treatment of cancers that included breast and prostate carcinomas. (bloodjournal.org)
  • Lovastatin acted by inhibiting both geranylgeranylation and farnesylation, and not by altering expression of key uptake receptors or by increasing binding of apoptotic cells to phagocytes. (jimmunol.org)
  • Indeed, direct inhibition of HMG-CoA reductase with lovastatin, a competitive inhibitor of this enzyme, induced a pronounced apoptotic response in neuroblastoma and acute myeloid leukemic cells. (aacrjournals.org)
  • Lovastatin induced a pronounced apoptotic response in cells derived from juvenile monomyelocytic leukemia, pediatric solid malignancies (rhabdomyosarcoma and medulloblastoma), and squamous cell carcinoma of the cervix and of the head and neck. (aacrjournals.org)
  • In this report, we demonstrate that the apoptotic properties of lovastatin are triggered by the open ring acid form that is a potent inhibitor of HMG-CoA reductase activity. (aacrjournals.org)
  • Transmission electron microscopic evaluation of TUNEL-confirmed apoptotic bodies in lovastatin-treated mammary carcinoma cells revealed many free 3′-OH ends of DNA in condensed chromatin within fragmented nuclei that occasionally assumed a characteristic half-moon shape. (oup.com)
  • Grapefruit and grapefruit juice may interact with lovastatin. (rxwiki.com)
  • It is recommended that people on lovastatin extended-release not drink grapefruit juice because it can increase the levels of lovastatin extended-release in the blood, which can increase the risk of developing serious muscle problems. (emedtv.com)
  • If you are being treated with lovastatin extended-release and want to continue drinking grapefruit juice, talk to your doctor about other cholesterol-lowering medications that you can take. (emedtv.com)
  • Studies of the centromere-associated protein mitosin revealed that treatment with lovastatin and paclitaxel resulted in increased mitosin levels and that lovastatin altered the association of mitosin with condensed chromosomes. (aacrjournals.org)
  • What Other Drugs Interact with Lovastatin? (rxlist.com)
  • There are many other drugs that can increase your risk of serious medical problems if you take them together with lovastatin and niacin. (cardiosmart.org)
  • Some drugs may increase the risk of side effects from lovastatin. (ahealthyme.com)
  • It's good to see that they are recognizing the risks of Lovastatin and similar drugs. (herbal-supplements-guide.com)
  • When you lower cholesterol naturally rather than take prescription medications you can avoid the many side effects of Lovastatin, Pravachol, Lipitor and similar drugs. (herbal-supplements-guide.com)
  • In recent years, studies involving statin drugs (e.g., lovastatin, simvastatin, etc.) have been successful in reducing cardiovascular disease and all-cause mortality. (dynamicchiropractic.com)
  • The following drugs can increase your risk of serious muscle problems if you take them together with lovastatin. (unclenoir.org)
  • Lovastatin is a cholesterol -lowering medication called a statin prescribed to treat elevated blood cholesterol levels. (rxlist.com)
  • This medication contains lovastatin. (rxlist.com)
  • Lovastatin and niacin may also be used for other purposes not listed in this medication guide. (cardiosmart.org)
  • People who have been taking Lovastatin have reported many different adverse reactions to the medication. (herbal-supplements-guide.com)
  • Lovastatin is a prescription medication used to treat high cholesterol levels and to prevent heart disease. (rxwiki.com)
  • Your lovastatin extended-release medication should be taken in the evening at bedtime. (emedtv.com)
  • These findings provide insight into the mechanisms underlying the cell cycle effects of lovastatin and support the development of a novel therapeutic strategy directed toward altering deleterious cell proliferation. (aacrjournals.org)
  • Given that both lovastatin and paclitaxel are used in the clinic and are capable of inducing cell cycle-specific effects, it is of great interest to determine whether combinations of these agents induce additive or supra-additive effects that may be harnessed for novel therapeutic applications. (aacrjournals.org)
  • These results provide in vitro support for the novel therapeutic approach of combining lovastatin and paclitaxel for altering abnormal cell proliferation in vivo . (aacrjournals.org)
  • 8 Therefore, lovastatin did not appear to be a viable therapeutic alternative in the treatment of human cancer. (bloodjournal.org)
  • Lovastatin serves as a potential therapeutic approach to mesangial proliferative disease. (asnjournals.org)
  • Thus, the relevance of these findings for the potential therapeutic effect of statins in RTT and the lack of replication studies of Buchovecky's and colleagues findings prompted us to re-assess the effects of Mecp2 deletion on brain and serum cholesterol levels, and the ability of lovastatin to prolong survival and rescue motor deficits in Mecp2 -null mice on a different background strain (B6), available from a commercial source. (elifesciences.org)
  • Lovastatin is a specific inhibitor of HMG-CoA reductase, the enzyme which catalyzes the conversion of HMG-CoA to mevalonate. (nih.gov)
  • The mechanism of action of lovastatin is inhibition of 3-hydroxy-3-methylglutaryl-coenzyme A reductase, an enzyme involved in the biosynthesis of cholesterol from acetyl-CoA. (pnas.org)
  • Researchers from the UCLA Henry Samueli School of Engineering and Applied Science have for the first time successfully reconstituted in the laboratory the enzyme responsible for producing the blockbuster cholesterol-lowering drug lovastatin. (redorbit.com)
  • The lovastatin-synthesizing enzyme is one of the most interesting but least understood of the polyketide synthases, which are found in filamentous fungi and which play a crucial role in the synthesis of "small molecule natural products" "" pharmacologically or biologically potent compounds produced by living organisms, many of which are the active ingredients in pharmaceuticals. (redorbit.com)
  • In this study, we studied the enzyme that makes a small-molecule precursor to lovastatin. (redorbit.com)
  • The enzyme used in Tang's study has seven active sites and catalyzes more than 40 different reactions that eventually result in an important precursor to lovastatin. (redorbit.com)
  • Lovastatin lowers hepatic cholesterol synthesis by competitively inhibiting HMG-CoA reductase, the enzyme that catalyzes the rate-limiting step in the cholesterol biosynthesis. (nextbio.com)
  • Lovastatin is an inhibitor of hydroxymethyl glutaryl (HMG)-CoA reductase, the rate-limiting enzyme in cholesterol synthesis. (pnas.org)
  • Lovastatin is an inhibitor of the enzyme hydroxymethylglutaryl coenzyme A (HMG-CoA) reductase (mevalonate:NADP + oxidoreductase [EC 1.1.1.34 ]) that catalyzes the reduction of HMG-CoA to mevalonate during synthesis of cholesterol ( 14 , 23 , 36 ). (asm.org)
  • Lovastatin induced a proteolytic activity that was able to cleave the enzyme poly(ADP-ribose) polymerase and the substrate Z-DEVD-AFC, which is modeled after the P 1 -P 4 amino acids of the poly(ADP-ribose) polymerase cleavage site. (aacrjournals.org)
  • Caspase-7 was the only detected interleukin 1β converting enzyme family protease with DEVD cleavage activity that exhibited lovastatin-induced mRNA up-regulation. (aacrjournals.org)
  • Two compounds, diallyl disulphide (DADS), an important component of garlic oil, and lovastatin, an inhibitor of a key enzyme of methanogenic Archaea, were selected on the basis of their in vitro anti-methanogenic potential. (sigmaaldrich.com)
  • In the present study, 110 fungal strains of Persian Type Culture Collection (PTCC) including some selected strains isolated in various screening projects were tested for their potentiality to produce lovastatin, a competitive inhibitor of 3-hydroxy-3-methylglutaryl-CoA reductase (HMG-CoA reduc-tase), the rate-limiting enzyme of cholesterol biosynthesis. (ac.ir)
  • Lovastatin is a cholesterol lowering agent isolated from a strain of Aspergillus terreus. (nih.gov)
  • Lovastatin is a secondary metabolite produced by Aspergillus terreus . (asm.org)
  • Lovastatin, monacolin J, monacolin L, and mevastatin can be produced by Monascus ruber ( 7 ), Penicillium brevicompactum , and Aspergillus terreus ( 1 , 36 ). (asm.org)
  • Lovastatin is a hexahydro naphthalene ester isolated from Aspergillus terreus broth. (chemicalbook.com)
  • Lovastatin, a natural product derived from Aspergillus terreus or Monascus ruber , has been widely used as cholesterol-lowing drug in the clinic. (jcancer.org)
  • Abstract -Lovastatin has been shown to reduce cholesterol esterification in cholesterol-loaded human macrophages. (ahajournals.org)
  • What Are Side Effects Associated with Using Lovastatin? (rxlist.com)
  • Kidney damage following doxorubicin exposure was not detectable under our experimental conditions.Moreover, lovastatin showed multiple inhibitory effects on doxorubicin-triggered hepatic expression of genes involved in oxidative stress response, drug transport, DNA repair, cell cycle progression and cell death. (nih.gov)
  • The in vitro and in vivo effects of lovastatin on fatty acid metabolism were studied in isolated rat hepatocytes. (nih.gov)
  • The in vitro and in vivo effects of lovastatin were not significantly different between periportal and perivenous hepatocytes. (nih.gov)
  • Effects of lovastatin and dietary cholesterol on sterol homeostasis in healthy human subjects. (jci.org)
  • The lovastatin-mediated inhibition of the proteasome suggests a unique mechanism for the chemopreventative effects of this agent seen in human cancer. (pnas.org)
  • If you don't ask about Lovastatin side effects, it's unlikely that your prescribing doctor will tell you what they are. (herbal-supplements-guide.com)
  • In these studies, we have examined the effects of combining lovastatin and paclitaxel (Taxol), a microtubule-stabilizing agent, in the human leukemia K562 and HL-60 cell lines. (aacrjournals.org)
  • The mechanism(s) of action underlying the cytotoxic effects of lovastatin are largely unknown and continues to be the focus of active investigation. (aacrjournals.org)
  • In this study, we evaluated the effects of combining lovastatin and paclitaxel in two human leukemia cell lines (K562 and HL-60) and investigated the mechanisms underlying the observed synergistic interaction. (aacrjournals.org)
  • 2)The inhibitory effects of lovastatin could be reversed almost completely by mevalonate, partially by farnesol. (koreamed.org)
  • The effects of the low-fat-low-cholesterol diet and lovastatin on lipoprotein levels were independent and additive. (unboundmedicine.com)
  • METHODS: The effects of lovastatin on lens transparency and on lens epithelial cell proliferation and structure have been investigated using organ-cultured rat lenses and cultured epithelial cells from human and rabbit lenses, respectively. (arvojournals.org)
  • Serious side effects have been reported with lovastatin. (rxwiki.com)
  • This is not a complete list of lovastatin side effects. (rxwiki.com)
  • Neurocytoprotective Effects of Aliphatic Hydroxamates from Lovastatin, a Secondary Metabolite from Monascus-Fermented Red Mold Rice, in 6-Hydroxydopamine (6-OHDA)-Treated Nerve Growth Factor (NGF)-Differentiated PC12 Cells. (sigmaaldrich.com)
  • Diallyl disulphide and lovastatin: effects on energy and protein utilisation in, as well as methane emission from, sheep. (sigmaaldrich.com)
  • RateADrug users have reported 3 Lovastatin side effects and 1 Lovastatin benefit. (rateadrug.com)
  • There are a number of side effects with lovastatin that you should report immediately to your healthcare provider. (rateadrug.com)
  • The lovastatin side effects mentioned below also occurred in more than one percent of people and more often in the group taking lovastatin. (rateadrug.com)
  • With a $66,714 grant from the FRAXA Research Foundation awarded over 2015-2017, Dr. Francois Corbin and Dr. Jean-Francois LePage at the Universite of Sherbrooke tested the safety and synergistic effects of lovastatin and minocycline in patients with Fragile X syndrome. (fraxa.org)
  • The team's multi-level preclinical validation strongly suggests that lovastatin could have disease-modifying effects in people with Fragile X. Fortunately, these results have been known to FRAXA for some time, having been presented at the 2011 FRAXA Investigators Meeting. (fraxa.org)
  • A recent study published in The American Journal of Clinical Nutrition showed that the cholesterol-lowering effect of newer dietary strategies (portfolio diet) could be similar to the effects of daily ingestion of 20 mg of lovastatin, in a population of 34 hyperlipidemic participants. (dynamicchiropractic.com)
  • Objective To investigate the effects of lovastatin on MAPK activity in MCF 7 breast cancer cells. (cnki.com.cn)
  • The aim of this study is to evaluate the effects of lovastatin on the cell viability and osteogenic differentiation of human gingiva-derived stem cells. (alliedacademies.org)
  • However, the effects of lovastatin on mesenchymal stem cells are not well revealed. (alliedacademies.org)
  • The effects of lovastatin, a potent inhibitor of hydroxymethylglutaryl-coenzyme A reductase, were studied in a mouse model of metastatic mammary cancer carrying a p53 mutation. (oup.com)
  • Laser scanning cytometric analyses further demonstrated that cancer cells in S and G 2 /M were particularly susceptible to the effects of lovastatin. (oup.com)
  • Some medicines can cause unwanted or dangerous effects when used with lovastatin. (unclenoir.org)
  • Lovastatin was found to be 2 times more potent than its predecessor, mevastatin, the first discovered statin. (drugbank.ca)
  • Lovastatin is potent inhibitor of 3-hydroxy-3-methylglutaryl-coenzyme A reductase (HMG-CoA reductase) that was initially isolated from A. terreus. (peprotech.com)
  • 3 4 Lovastatin is also a potent inducer of growth arrest at the G1/S boundary in a wide variety of normal and tumor-derived cell lines. (bloodjournal.org)
  • Moreover, we explore and compare the mechanism of action of lovastatin with the most potent statin, cerivastatin. (aacrjournals.org)
  • Lovastatin appeared to exert its positive effect on efferocytosis by inhibiting RhoA, because it 1) decreased membrane localization of RhoA, to a greater extent than Rac-1, and 2) prevented impaired efferocytosis by lysophosphatidic acid, a potent inducer of RhoA. (jimmunol.org)
  • Mevalonic acid (1 mmol/L) reversed lovastatin-induced inhibition of cell growth if it was added with lovastatin (2.5 micrograms/mL). (biomedsearch.com)
  • Lovastatin is a cholesterol-lowering agent that belongs to the class of medications called statins. (drugbank.ca)
  • Lovastatin belongs to the family of medications known as lipid metabolism regulators . (medbroadcast.com)
  • After oral ingestion, lovastatin, which is an inactive lactone, is hydrolyzed to the corresponding β-hydroxyacid form. (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)
  • In addition to lowering serum LDL cholesterol, lovastatin significantly lowered biliary secretion of cholesterol, fecal output of endogenous neutral sterols, cholesterol balance, and systemic cholesterol input (the sum of cholesterol synthesis and absorbed dietary cholesterol). (jci.org)
  • Inhibition of pancreatic adenocarcinoma cell growth by lovastatin. (biomedsearch.com)
  • Lastly, mevalonate (used to rescue cells from lovastatin arrest) unexpectedly abrogates the lactacystin and lovastatin pro-drug inhibition of the proteasome. (pnas.org)
  • Lens epithelial cells (both human and rabbit) demonstrated extensive morphologic changes and inhibition of proliferation when treated with lovastatin. (arvojournals.org)
  • To determine the inhibitory mechanisms of mesangial cell proliferation by lovastatin, the cyclin-dependent kinase (CDK) activity, and expression of CDK inhibitor (p27Kip1, p21Cip1, and p16INK4) mRNA and protein were measured. (asnjournals.org)
  • Modulation of these pathways may mediate, in part, the inhibitory activity of lovastatin on breast cancer. (jcancer.org)
  • Like mevastatin, lovastatin is structurally similar to hydroxymethylglutarate (HMG), a substituent of HMG-Coenzyme A (HMG-CoA), a substrate of the cholesterol biosynthesis pathway via the mevalonic acid pathway. (drugbank.ca)
  • A chemically defined medium was developed in order to investigate the influence of carbon and nitrogen sources on lovastatin biosynthesis. (asm.org)
  • Among several organic and inorganic defined nitrogen sources metabolized by A. terreus , glutamate and histidine gave the highest lovastatin biosynthesis level. (asm.org)
  • Despite the knowledge of the genes and the enzymes involved in the biosynthetic pathway, little is known about the regulation and the physiology of lovastatin biosynthesis. (asm.org)
  • In addition, lovastatin biosynthesis was initiated only when assimilation of the carbon source was limited. (asm.org)
  • Overall, the data show that lovastatin is hepatoprotective following genotoxic stress induced by anthracyclines. (nih.gov)
  • In this study, we show that lovastatin increased efferocytosis in vitro in an 3-hydroxyl-3-methylglutaryl coenzyme A (HMG-CoA) reductase-dependent manner. (jimmunol.org)
  • The ability of lovastatin to cause growth arrest and its reversibility has led to its use as a cell-synchronizing agent in vitro. (bloodjournal.org)
  • The aim of this study was to enhance the activity of lovastatin for potential use as a treatment for neuronal degeneration in Parkinson's disease. (sigmaaldrich.com)
  • This study demonstrated the potential effect of simvastatin and lovastatin on the metabolism of sinomenine for the first time. (ovid.com)
  • Lovastatin is a competitive inhibitor of HMG-CoA reductase with a binding affinity 20,000 times greater than HMG-CoA. (drugbank.ca)
  • With lovastatin, the rate is approximately 1/1.14 million patient-treatment years, which is 9% of the background rate of all causes of ALF and approximately equal to the background rate of idiopathic ALF. (nih.gov)
  • The primary uses of lovastatin is for the treatment of dyslipidemia and the prevention of cardiovascular disease . (wikipedia.org)
  • Lovastatin should be used in addition to dietary modifications as part of a treatment plan to lower cholesterol levels when the response to diet and other non-pharmacological measures alone have been inadequate to reduce cardiovascular risk. (rxlist.com)
  • Acute and subacute hepatotoxicities were analyzed with or without lovastatin co-treatment. (nih.gov)
  • Hepatoprotection by lovastatin was due to a reduced induction of DNA damage following doxorubicin treatment. (nih.gov)
  • Similarly, removal of lovastatin from the medium within 24 hours after treatment allowed recovery of cell growth. (biomedsearch.com)
  • Lovastatin should be used in addition to a diet restricted in saturated fat and cholesterol as part of a treatment strategy to lower total-C and LDL-C to target levels when the response to diet and other nonpharmacological measures alone has been inadequate to reduce risk. (prescriptiondrugs.com)
  • Each of the 97 patients completing the study (58 men and 39 women) underwent four consecutive nine-week periods of treatment according to a randomized, balanced design: a high-fat diet-placebo period, a low-fat diet-placebo period, a high-fat diet-lovastatin period, and a low-fat diet-lovastatin period. (unboundmedicine.com)
  • Treatment with lovastatin revealed the increment of both CDK2- and CDK4-bound-p27Kip1. (asnjournals.org)
  • p = 0.02) with DADS than without supplementation, and the lovastatin treatment ranged in between. (sigmaaldrich.com)
  • Dr. Corbin also ran the first clinical trial of lovastatin as a potential treatment for Fragile X Syndrome, funded by FRAXA in 2012 for $44,000. (fraxa.org)
  • In nonloaded cells, by contrast, the cholesteryl esters of unsaturated fatty acids tended to increase after lovastatin treatment. (ahajournals.org)
  • Total (free plus esterified) cellular cholesterol content in nonloaded cells fell by 18% with 12-μmol/L lovastatin treatment but did not change in cholesterol-loaded cells. (ahajournals.org)
  • Apolipoprotein (apo) E mRNA levels increased but apoE secretion into the medium decreased with lovastatin treatment in both cholesterol-loaded and nonloaded cells. (ahajournals.org)
  • The benefit of lovastatin treatment was consistently observed across multiple subgroups of risk defined by this model. (nyp.org)
  • Patients then applied topical cholesterol/lovastatin twice daily to a unilaterally defined treatment area for up to 3 months. (northwestern.edu)
  • Treatment with topical cholesterol/lovastatin (but not cholesterol alone) resulted in near complete clearance of disseminated superficial actinic porokeratosis lesions after 4 weeks of therapy and moderate improvement of porokeratosis palmaris et plantaris disseminata lesions and linear porokeratosis lesions. (northwestern.edu)
  • Choate, Keith A. / Topical cholesterol/lovastatin for the treatment of porokeratosis : A pathogenesis-directed therapy . (northwestern.edu)
  • When added in vitro to cell incubations, lovastatin stimulated de novo fatty acid synthesis and acetyl-CoA carboxylase activity, whereas fatty acid synthase activity was unaffected. (nih.gov)
  • Lovastatin had no effect on the synthesis and secretion of triacylglycerols and phospholipids in the form of very low density lipoproteins (VLDL). (nih.gov)
  • When rats were fed a diet supplemented with 0.1% (w/w) lovastatin for one week, both acetyl-CoA carboxylase activity and de novo fatty acid synthesis were reduced compared to pair-fed controls, whereas fatty acid synthase activity was unaffected. (nih.gov)
  • Judging from these data, the primary action of lovastatin is to lower cholesterol synthesis and systemic cholesterol input, the main compensatory response being reduced biliary cholesterol secretion. (jci.org)
  • RESULTS: 1)Lovastatin inhibited DNA synthesis and cell proliferation in a dose-dependent manner. (koreamed.org)
  • Supplementation of the medium with DL-mevalonic acid (a precursor of isoprenoids whose synthesis is inhibited by lovastatin) prevented the lovastatin-induced changes in whole lenses or in lens epithelial cell cultures, whereas supplementation with cholesterol had no such effect. (arvojournals.org)
  • For cultures on glucose and glutamate, lovastatin synthesis initiated when glucose consumption levelled off. (asm.org)
  • Lovastatin decreases coenzyme Q levels in humans. (pnas.org)
  • The bicyclic portion of lovastatin binds to the coenzyme A portion of the active site. (nextbio.com)
  • Lovastatin had no effect on the binding or uptake of acetylated low density lipoprotein, acyl coenzyme A:cholesterol acyltransferase (ACAT) activity, the secretion of [ 3 H]cholesterol into the medium, or lysosomal hydrolysis of cholesteryl esters. (ahajournals.org)
  • That the lovastatin-induced impairment of proliferation is reversed by mevalonic acid, but not cholesterol ( 8 ), strongly suggests that the effect is attributable to alterations in protein isoprenylation. (aacrjournals.org)
  • In cholesterol-loaded cells, lovastatin reduced the cholesteryl esters of unsaturated but not those of saturated fatty acids. (ahajournals.org)
  • It is a combination of the vitamin niacin and the statin drug lovastatin . (wikipedia.org)
  • The lipid lowering drug lovastatin protects against doxorubicin-induced hepatotoxicity. (nih.gov)
  • June 25, 2014 - Doctor's Best is voluntarily recalling Red Yeast Rice supplements because they contain lovastatin , a prescription statin that is used to lower cholesterol levels. (schmidtlaw.com)
  • The highest lovastatin content was observed in Hericium erinaceus (FB) (14.38 μg/g) and Ganoderma lucidum (FB) (11.54 μg/g). (begellhouse.com)
  • Each blue, octagonal, flat-faced, bevelled-edged tablet, marked 'LS' over '20' on one side and a chevron on the other, contains lovastatin 20 mg. (medbroadcast.com)
  • Someone posted a link to an article that mentioned the FDA's banning of red yeast rice because it naturally contains 'lovastatin. (ronpaulforums.com)
  • PURPOSE: To investigate the biochemical mechanisms involved in the cataract induced by lovastatin, a commonly used cholesterol-lowering agent. (arvojournals.org)
  • Of significance, in the acute myeloid leukemia, but not the acute lymphocytic leukemia cell lines, lovastatin-induced cytotoxicity was pronounced even at the physiological relevant concentrations of this agent. (bloodjournal.org)
  • Cells derived from acute lymphocytic leukemia are only weakly sensitive to lovastatin cytotoxicity but show robust response to cerivastatin. (aacrjournals.org)