Substances used to lower plasma CHOLESTEROL levels.

Comparison of synthetic saponin cholesterol absorption inhibitors in rabbits: evidence for a non-stoichiometric, intestinal mechanism of action. (1/2109)

The hypocholesterolemic activities of pamaqueside and tiqueside, two structurally similar saponins, were evaluated in cholesterol-fed rabbits. The pharmacological profiles of the saponins were virtually identical: both dose-dependently decreased the intestinal absorption of labeled cholesterol 25-75%, increased fecal neutral sterol excretion up to 2.5-fold, and decreased hepatic cholesterol content 10-55%. High doses of pamaqueside (>5 mg/kg) or tiqueside (>125 mg/kg) completely prevented hypercholesterolemia. Decreases in plasma and hepatic cholesterol levels were strongly correlated with increased neutral sterol excretion. Ratios of neutral sterol excreted to pamaqueside administered were greater than 1:1 at all doses, in opposition to the formation of a stoichiometric complex previously suggested for tiqueside and other saponins. Ratios in tiqueside-treated rabbits were less than unity, a reflection of its lower potency. Pamaqueside-treated rabbits exhibited a more rapid decline in plasma cholesterol concentrations than control animals fed a cholesterol-free diet, indicating that the compound also inhibited the absorption of biliary cholesterol. Intravenous administration of pamaqueside had no effect on plasma cholesterol levels despite plasma levels twice those observed in rabbits given pamaqueside orally. These data indicate that pamaqueside and tiqueside induce hypocholesterolemia by blocking lumenal cholesterol absorption via a mechanism that apparently differs from the stoichiometric complexation of cholesterol hypothesized for other saponins.  (+info)

Role of cholesterol ester mass in regulation of secretion of ApoB100 lipoprotein particles by hamster hepatocytes and effects of statins on that relationship. (2/2109)

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)

Effects of 2 low-fat stanol ester-containing margarines on serum cholesterol concentrations as part of a low-fat diet in hypercholesterolemic subjects. (3/2109)

BACKGROUND: Full-fat sitostanol ester-containing margarine reduces serum total and LDL cholesterol, but the effect of plant stanol ester-containing margarine as part of a low-fat, low-cholesterol diet has not been studied. OBJECTIVE: We investigated the cholesterol-lowering effects of 2 novel, low-fat stanol ester-containing margarines as part of a low-fat diet recommended for hypercholesterolemic subjects. DESIGN: In a parallel, double-blind study, 55 hypercholesterolemic subjects were randomly assigned after a 4-wk high-fat diet (baseline) to 3 low-fat margarine groups: wood stanol ester-containing margarine (WSEM), vegetable oil stanol ester-containing margarine (VOSEM), and control margarine (no stanol esters). The groups consumed the margarines for 8 wk as part of a diet resembling that of the National Cholesterol Education Program's Step II diet. The daily mean total stanol intake was 2.31 and 2.16 g in the WSEM and VOSEM groups, respectively. RESULTS: During the experimental period, the reduction in serum total cholesterol was 10.6% (P < 0.001) and 8.1% (P < 0.05) greater and in LDL cholesterol was 13.7% (P < 0.01) and 8.6% (P = 0.072) greater in the WSEM and VOSEM groups, respectively, than in the control group. Serum campesterol concentrations decreased 34.5% and 41.3% (P < 0.001) in the WSEM and VOSEM groups, respectively. Serum HDL cholesterol, sitostanol, campestanol, beta-carotene, and fat-soluble vitamin concentrations did not change significantly from baseline. CONCLUSIONS: We conclude that the low-fat, plant stanol ester-containing margarines are effective cholesterol-lowering products in hypercholesterolemic subjects when used as part of a low-fat, low-cholesterol diet. They offer an additional, clinically significant reduction in serum cholesterol concentrations to that obtained with a low-fat diet alone.  (+info)

Effect of long term simvastatin administration as an adjunct to ursodeoxycholic acid: evidence for a synergistic effect on biliary bile acid composition but not on serum lipids in humans. (4/2109)

BACKGROUND: Stimulated bile acid synthesis preferentially utilises newly synthesised cholesterol, raising the possibility that combination of simvastatin (an inhibitor of cholesterol synthesis) with ursodeoxycholic acid (UDCA; a stimulator of bile acid synthesis) may result in reduced bile acid synthesis and greater enrichment of the pool with UDCA than that achieved with UDCA treatment alone. AIMS: To investigate the effect of simvastatin and UDCA given alone and in combination on serum and biliary lipid and biliary bile acid composition. METHODS: Eighteen patients with primary non-familial hypercholesterolaemia were studied during treatment with simvastatin 20 mg/day, UDCA 10 mg/kg/day, and a combination of the two drugs. Each regimen was given in random order for three months following a three month lead in period. RESULTS: Simvastatin significantly reduced serum low density lipoprotein (LDL) cholesterol but biliary cholesterol concentration remained unchanged. Combination of the two drugs had no synergistic effect on serum cholesterol concentration, but significantly increased the proportion of UDCA in the bile acid pool from 35% during UDCA to 48% during combination treatment (p<0.04). CONCLUSIONS: Results showed that: (1) simvastatin reduces serum LDL cholesterol but has no effect on biliary cholesterol concentration, supporting the concept that newly synthesised cholesterol is not the preferential source for biliary cholesterol; and (2) combination of simvastatin with UDCA has the predicted effect of enhancing the proportion of UDCA in the pool. This effect may be of benefit in the treatment of cholestatic liver diseases.  (+info)

Effect of the hypocholesterolemic agent YM-16638 on cholesterol biosynthesis activity and apolipoprotein B secretion in HepG2 and monkey liver. (5/2109)

YM-16638 ([[5-[[3-(4-acetyl-3-hydroxy-2-propylphenoxy)propyl]thio]-1,3,4-++ +thiadiazol-2-yl] thio] acetic acid) showed a strong hypocholesterolemic effect in humans and monkeys. To clarify the mechanism of this hypocholesterolemic effect, the action of YM-16638 on cholesterol biosynthesis in the cultured human hepatoma cell line HepG2 and cynomolgus monkey liver was examined. Cholesterol biosynthesis activity derived from [14C]acetic acid, [3H/14C]mevalonic acid or [14C]isopentenyl pyrophosphate substrates was significantly decreased, but not that from [3H]farnesyl pyrophosphate or [3H]squalene substrates in HepG2 cells treated with YM-16638. Simultaneously, treatment of these cells with YM-16638 changed neither the rate of apolipoprotein B synthesis from [35S]methionine nor its secretion. In addition, the activities of hepatic cholesterol biosynthesis enzymes HMG-CoA reductase, mevalonate kinase (MK), isopentenyl pyrophosphate isomerase (IPPI), farnesyl pyrophosphate synthase (FPPS), squalene synthase and squalene epoxidase were measured in monkeys fed a diet supplemented with YM-16638. Among these enzymes, MK, IPPI and FPPS activities in the YM-16638-treated group significantly decreased by 38%, 56% and 30%, respectively, when compared to those from control animals receiving no drug treatment. These results indicate that YM-16638 has the characteristics of a cholesterol biosynthesis inhibitor.  (+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. (6/2109)

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. (7/2109)

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)

The effects of pravastatin on hospital admission in hypercholesterolemic middle-aged men: West of Scotland Coronary Prevention Study. (8/2109)

OBJECTIVES: The purpose of the study was to assess the effect of lipid reduction with pravastatin on hospital admissions in middle-aged men with hypercholesterolemia in the West of Scotland Coronary Prevention Study. BACKGROUND: A prospective, randomized controlled trial was undertaken in primary care centers in the West of Scotland. METHODS: A total of 6,595 participants randomized to receive pravastatin 40 mg or placebo daily were followed up for a mean of 4.9 years (range 3.5 to 6.1 years). Analysis of hospital admissions was undertaken according to the "intention to treat" principle both for cardiovascular diseases and noncardiovascular diseases (including malignant neoplasms, psychiatric diagnoses, trauma and other causes). A secondary analysis of hospitalization in patients who were > or = 75% compliant was performed. RESULTS: During the trial, 2,198 (33%) of the 6,595 men were admitted to hospital on 4,333 occasions, of which 1,234 (28%) were for cardiovascular causes. Pravastatin reduced the number of subjects requiring hospital admission for cardiovascular causes by 21% (95% CI [confidence interval] 9 to 31, p = 0.0008) overall, and by 27% (95% CI 15 to 38) in compliant participants. The number of admissions per 1,000 subject-years for cardiovascular disease was reduced by 10.8 (95% CI 4 to 17.4, p = 0.0013) in all subjects, and by 15.6 (95% CI 8.3 to 23, p < 0.0001) in compliant participants. Pravastatin had no significant influence on hospital admission for any noncardiovascular diagnostic category. There were 13.4 fewer admissions per 1,000 subject-years for all causes in the pravastatin-treated group (95% CI -0.4 to 27.3, p = 0.076). No significant difference in duration of hospital stay was found between the pravastatin and placebo patients in any diagnostic group. CONCLUSIONS: Pravastatin therapy reduced the burden of hospital admissions for cardiovascular disease, without any adverse effect on noncardiovascular hospitalization.  (+info)

Anticholesteremic agents are a class of medications that are used to lower the levels of cholesterol and other fats called lipids in the blood. These medications work by reducing the production of cholesterol in the body, increasing the removal of cholesterol from the bloodstream, or preventing the absorption of cholesterol in the digestive tract.

There are several types of anticholesteremic agents, including:

1. Statins: These medications work by blocking a liver enzyme that is necessary for the production of cholesterol. Examples of statins include atorvastatin, simvastatin, and rosuvastatin.
2. Bile acid sequestrants: These medications bind to bile acids in the digestive tract and prevent them from being reabsorbed into the bloodstream. This causes the liver to produce more bile acids, which in turn lowers cholesterol levels. Examples of bile acid sequestrants include cholestyramine and colesevelam.
3. Nicotinic acid: Also known as niacin, this medication works by reducing the production of very low-density lipoproteins (VLDL) in the liver, which are a major source of bad cholesterol.
4. Fibrates: These medications work by increasing the removal of cholesterol from the bloodstream and reducing the production of VLDL in the liver. Examples of fibrates include gemfibrozil and fenofibrate.
5. PCSK9 inhibitors: These are a newer class of medications that work by blocking the action of a protein called PCSK9, which helps regulate the amount of cholesterol in the blood. By blocking PCSK9, these medications increase the number of LDL receptors on the surface of liver cells, which leads to increased removal of LDL from the bloodstream.

Anticholesteremic agents are often prescribed for people who have high cholesterol levels and are at risk for heart disease or stroke. By lowering cholesterol levels, these medications can help reduce the risk of heart attack, stroke, and other cardiovascular events.

... antilipemic agents MeSH D27.505.954.230.202 - anticholesteremic agents MeSH D27.505.954.230.202.370 - hydroxymethylglutaryl-coa ... antilipemic agents MeSH D27.505.519.186.071.202 - anticholesteremic agents MeSH D27.505.519.186.071.202.370 - ... antiviral agents MeSH D27.505.954.122.388.077 - anti-retroviral agents MeSH D27.505.954.122.388.077.088 - anti-hiv agents MeSH ... tocolytic agents MeSH D27.505.954.016 - anti-allergic agents MeSH D27.505.954.122 - anti-infective agents MeSH D27.505.954.122. ...
... antibiotics, antifungals, cytostatics, anticholesteremic, antiparasitics, coccidiostats, animal growth promoters and ... The cholesterol lowering agent lovastatin Discodermolide Aflatoxin Usnic acid Anthracimycin Anthramycin Olivetolic acid ( ... and azithromycin The antihelminthics ivermectin Ansamycins The antitumor agents geldanamycin and macbecin, The antibiotic ... nystatin and pimaricin Polyethers The antibiotic monensin Tetracyclines The antibiotic agent doxycycline Acetogenins bullatacin ...
Anticholesteremic Agents / therapeutic use* * Antihypertensive Agents / therapeutic use * Atorvastatin * Cholesterol / blood* * ...
Anti-Inflammatory Agents. 4. 16. Anticholesteremic Agents. 3. 15. Antihypertensive Agents. 1. 10. ... Grapefruit seed extract might be used as an anti-biofilm agent that is effective against S. aureus and E. coli.Jul 31, 2019. ... Grapefruit Seed Extract is a Powerful in vitro Agent Against Motile and Cystic Forms of Borrelia burgdorferi sensu lato.Jun 01 ... Pharmacological Actions : Anti-Bacterial Agents, Quorum Sensing Inhibition. Additional Keywords : Bacterial Infections: ...
Pharmacological Actions : Anticholesteremic Agents, Gastrointestinal Agents. [+] Blackberries improve motor and cognitive ... Pharmacological Actions : Antigiardial agents, Antiparasitic Agents. Additional Keywords : Antiparasitic Agents, Drug: ... Pharmacological Actions : Anti-Inflammatory Agents, Antioxidants, Neuroprotective Agents. Additional Keywords : Anti- ... Pharmacological Actions : Antioxidants, Hypoglycemic Agents, Malondialdehyde Down-regulation, Pancreato Protective Agents, ...
Anticholesteremic Agents / adverse effects * Anticholesteremic Agents / therapeutic use * Biomarkers / blood * Cholesterol, LDL ...
... antilipemic agents MeSH D27.505.954.230.202 - anticholesteremic agents MeSH D27.505.954.230.202.370 - hydroxymethylglutaryl-coa ... antilipemic agents MeSH D27.505.519.186.071.202 - anticholesteremic agents MeSH D27.505.519.186.071.202.370 - ... antiviral agents MeSH D27.505.954.122.388.077 - anti-retroviral agents MeSH D27.505.954.122.388.077.088 - anti-hiv agents MeSH ... tocolytic agents MeSH D27.505.954.016 - anti-allergic agents MeSH D27.505.954.122 - anti-infective agents MeSH D27.505.954.122. ...
Anticholesteremic Agents/pharmacology. *Atorvastatin. *Bile Acids and Salts/pharmacology. *Boron Compounds/metabolism ...
Anticholesteremic Agent Chemistry 66% * 3-hydroxy-3-methylglutaryl-coenzyme A Medicine & Life Sciences 56% ...
Keywords: Anticholesteremic Agents, Drug Utilization, Female, Humans, Hydroxymethylglutaryl-CoA Reductase Inhibitors, Male, ...
Keywords: Anticholesteremic Agents; Chemistry, Pharmaceutical; Crystallization; Drug Stability; Drug Storage; Excipients; ...
Singh, S., Goo, J., Gajulapati, V., Chang, T. S., Lee, K. & Choi, Y., 2016 May 1, In: Anti-Cancer Agents in Medicinal Chemistry ... Total Synthesis of the Neuroprotective Agent Cudraisoflavone J. Lu, Q., Harmalkar, D. S., Quan, G., Kwon, H., Cho, J., Choi, Y. ...
... inhibitors are currently in clinical development as potential lipid-lowering and antiatherosclerotic agents. We investigated ...
Anticholesteremic Agent 26% * Elimination Half-Life 24% * Acid 23% * Controlled Substance 20% ...
Anticholesteremic Agents 23% * Autosomal Dominant Polycystic Kidney 22% * Mutation 21% Chemical Compounds. * Protein 64% ...
Anticholesteremic Agents [D27.505.519.186.071.202] Anticholesteremic Agents * Hydroxymethylglutaryl-CoA Reductase Inhibitors [ ... Agents that inhibit Proprotein Convertase Subtilisin/Kexin Type 9 (see PROPROTEIN CONVERTASE 9 (PCSK9)), an enzyme that plays ... Agents that inhibit Proprotein Convertase Subtilisin/Kexin Type 9 (see PROPROTEIN CONVERTASE 9 (PCSK9)), an enzyme that plays ...
Anticholesteremic Agents -- therapeutic use. Azetidines -- therapeutic use. Enzyme Inhibitors -- therapeutic use. ...
Anticholesteremic Agents Medicine & Life Sciences 23% * Cholesterol Medicine & Life Sciences 23% * Animal Disease Models ... Despite advances in neuroimaging, surgical techniques, radiotherapy and the introduction of new chemotherapeutic agents, up to ... In addition, Hh pathway blockade sensitized medulloblastoma to the effects of the proapoptotic, cholesterol-lowering agent ... Despite advances in neuroimaging, surgical techniques, radiotherapy and the introduction of new chemotherapeutic agents, up to ...
AllylamineAnticholesteremic AgentsAzetidinesCardiovascular DiseasesColesevelam HydrochlorideDrug Therapy, CombinationEzetimibe ...
Anticholesteremic Agents. *Hypolipidemic Agents. *Apolipoproteins B. *Hyperlipoproteinemia Type II. *Lipoproteins. *Cholesterol ...
Anticholesteremic Agents, Antihypertensive Agents, Aspirin, Cardiovascular Diseases, Drug Combinations, Humans, Placebo Effect ...
Anticholesteremic Agents, Cause of Death, Cholesterol, Coronary Disease, Diet, Humans, Mortality. * Freedom of Information ...
Add ezetimibe Ezetimibe An azetidine derivative and anticholesteremic agent that inhibits intestinal sterol absorption. It is ... If further control is needed despite statin + ezetimibe Ezetimibe An azetidine derivative and anticholesteremic agent that ... and anticholesteremic agent that is used to reduce serum levels of ldl-cholesterol; apolipoprotein b; and triglycerides. It is ... and anticholesteremic agent that is used to reduce serum levels of ldl-cholesterol; apolipoprotein b; and triglycerides. It is ...
Analysis of Variance, Anticholesteremic Agents, Brain, Case-Control Studies, Fenfluramine, Humans, Hypercholesterolemia, Lipids ...
Aged, Aged, 80 and over, Anticholesteremic Agents, Cardiovascular Diseases, Cholesterol, LDL, Clinical Trials as Topic, Humans ...
Anticholesteremic Agents * Biological Transport * Cholesterol, HDL Explore _. Co-Authors (1) People in Profiles who have ...
Aged, Anticholesteremic Agents, Antioxidants, Ascorbic Acid, Coronary Disease, Double-Blind Method, Female, Humans, Male, ...
... and ANTICHOLESTEREMIC AGENT that is used to reduce serum levels of LDL-CHOLESTEROL; APOLIPOPROTEIN B; and TRIGLYCERIDES. It is ...
Anticholesteremic Agents, Cholesterol, LDL, Clinical Trials as Topic, Coronary Disease, Drug-Related Side Effects and Adverse ...
Aged, Antibodies, Monoclonal, Antibodies, Monoclonal, Humanized, Anticholesteremic Agents, Atherosclerosis, Cardiovascular ...
Adult, Aged, Aged, 80 and over, Anticholesteremic Agents, Cause of Death, Cholesterol, Cholesterol, LDL, Diabetes Mellitus, ...
Adult, Aged, Aged, 80 and over, Anticholesteremic Agents, Arterial Occlusive Diseases, Cholesterol, HDL, Cholesterol, LDL, ...
  • Unripe Rubus coreanus shows great promise as a therapeutic agent for subjects with borderline-high total blood cholesterol levels. (greenmedinfo.com)
  • In addition, Hh pathway blockade sensitized medulloblastoma to the effects of the proapoptotic, cholesterol-lowering agent lovastatin. (johnshopkins.edu)
  • Agents that inhibit Proprotein Convertase Subtilisin/Kexin Type 9 (see PROPROTEIN CONVERTASE 9 (PCSK9)), an enzyme that plays an important role in the degradation of the LDL receptors. (bvsalud.org)
  • Treatment is with statins, anti-hypertensive and antiplatelet agents, and, in some cases (depending on the degree of stenosis and associated symptoms) , surgical revascularization. (lecturio.com)
  • Despite advances in neuroimaging, surgical techniques, radiotherapy and the introduction of new chemotherapeutic agents, up to 30% of all patients diagnosed with medulloblastoma will die from their disease, thus underscoring the need for more effective treatments. (johnshopkins.edu)
  • An allylamine derivative that binds BILE ACIDS in the intestine and is used as an ANTICHOLESTEREMIC AGENT in the treatment of HYPERCHOLESTEROLEMIA and HYPERLIPIDEMIAS . (nih.gov)
  • This is a target mechanism in humans of some ANTINEOPLASTIC AGENTS and ANTI-OBESITY AGENTS and of some ANTI-INFECTIVE AGENTS which interfere with CELL WALL and CELL MEMBRANE formation. (nih.gov)
  • They represent an important class of synthetic antibiotic agents. (uchicago.edu)