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Cushing’s syndrome is a set of symptoms and clinical signs caused by a prolonged exposure to excessive levels of cortisol or other glucocorticoids from endogenous or exogenous sources. It has a female predominance and usually affects adults between 20 and 50 years of age. The global incidence of endogenous Cushing’s syndrome is 0, 7 to 2, 4 cases per year. This is a severe condition associated with an elevated mortality rate which makes it important to treat. The goal of the treatment is to remove, if possible, the cause of hypercortisolism in order to normalize the cortisolemia, reverse the clinical picture and prevent comorbidities. The recent arrival on the market of drugs indicated for the treatment of Cushing’s syndrome now offers to the patients the chance to be treated while waiting to undergo surgery, in case of prior surgical failure or in case of unresectable, metastasic or occult tumor. The three most currently used oral drugs are ketoconazole, metyrapone, and mifepristone. The former two inhibit cortisol synthesis while the latter is a competitive glucocorticoid receptor (GR-II) antagonist. The aim of this thesis was to compare these three molecules in terms of efficacy and safety. It appears that all of them have advantages and disadvantages, and that not only should be the treatment be chosen considering the characteristics of these drugs but also according to those of the patients, such as their sex, the degree of hypercortisolism or the already existing complications. Le syndrome de Cushing est un ensemble de symptômes et de signes cliniques provoqués par une exposition prolongée à des taux excessifs de cortisol ou d'autres glucocorticoïdes de sources endogène ou exogène. Il a une prédominance féminine et touche généralement les adultes âgés de 20 à 50 ans. L'incidence mondiale du syndrome de Cushing endogène est de 0,7 à 2,4 cas par an. JI s'agit d'une affection sévère associée à une élévation du taux de mortalité, c'est pourquoi il est important de la traiter. Le but du traitement est de supprimer, si possible, la cause de l'hypercorticisme afin de normaliser la cortisolémie, d'inverser le tableau clinique et de prévenir les comorbidités. La mise sur le marché récente de traitements médicamenteux ayant pour indication le traitement du syndrome de Cushing offre désormais aux patients la possibilité d'être traités dans l'attente d'une opération chirurgicale, en cas d'échec d'une chirurgie antérieure ou encore lorsque l'on a affaire à une tumeur non résécable, métastatique ou occulte.Les trois traitements médicamenteux par voie orale les plus utilisés actuellement sont le kétoconazole, la métyrapone et la mifépristone. Les deux premiers sont des inhibiteurs de la synthèse du cortisol et le troisième est un antagoniste compétitif du récepteur aux glucocorticoïdes (GR-Il). Le but de ce mémoire était de comparer ces trois molécules en termes d'efficacité et de sécurité. Il en ressort que chacune d'entre elles possède des avantages et des inconvénients, et que le traitement ne doit pas être choisi uniquement vis-à-vis des caractéristiques de ces médicaments mais aussi en fonction des celles propres aux patients, telles que le sexe, le degré d'hypercorticisme ou encore les complications déjà existantes.

Ketoconazole --- Metyrapone --- Mifepristone --- Cushing Syndrome

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Mycoses --- Antifungal Agents --- Ketoconazole --- drug therapy --- therapeutic use --- analogs & derivatives

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Anthelmintiques --- Antifongiques --- Antimycosiques --- Azoles (1h- 1-substitues monocycliques) --- Benzimidazole --- Chimiotherapie --- Imidazoles --- Ketoconazole --- Maladies fongiques --- Mycoses --- Quinuclidine (derives)

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Drug–drug interactions (DDIs) cause a drug to affect other drugs, leading to reduced drug efficacy or increased toxicity of the affected drug. Some well-known interactions are known to be the cause of adverse drug reactions (ADRs) that are life threatening to the patient. Traditionally, DDI have been evaluated around the selective action of drugs on specific CYP enzymes. The interaction of drugs with CYP remains very important in drug interactions but, recently, other important mechanisms have also been studied as contributing to drug interaction including transport- or UDP-glucuronyltransferase as a Phase II reaction-mediated DDI. In addition, novel mechanisms of regulating DDIs can also be suggested. In the case of the substance targeted for interaction, not only the DDIs but also the herb–drug or food–drug interactions have been reported to be clinically relevant in terms of adverse side effects. Reporting examples of drug interactions on a marketed drug or studies on new mechanisms will be very helpful for preventing the side effects of the patient taking these drugs. This Special Issue aims to highlight current progress in understanding both the clinical and nonclinical interactions of commercial drugs and the elucidation of the mechanisms of drug interactions.

tadalafil --- ticagrelor --- drug-drug interaction --- pharmacokinetics --- plasma concentration --- CYP3A4 --- Loxoprofen --- CYP3A --- Dexamethasone --- Ketoconazole --- CYP2D6 --- O-desmethyltramadol --- physiologically-based pharmacokinetics --- tramadol --- (‒)-sophoranone --- CYP2C9 --- potent inhibition --- in vitro --- in vivo --- drug interaction --- low permeability --- high plasma protein binding --- biflavonoid --- cytochrome P450 --- drug interactions --- selamariscina A --- uridine 5′-diphosphoglucuronosyl transferase --- tissue-specific --- systemic exposure --- P-glycoprotein (P-gp) --- organic anion transporting polypeptide 1A2 (OATP1A2) --- Rumex acetosa --- fexofenadine --- chronic kidney disease --- drug–drug interactions --- polypharmacy --- adverse drug reactions --- Lexicomp --- subset analysis --- signal detection algorithms --- spontaneous reporting systems --- mechanism-based inhibition --- competitive inhibition --- non-competitive inhibition --- substrate --- inhibitor --- cytochromes P450 --- OATP1B1 --- OATP1B3 --- tyrosine kinase inhibitors --- drug-drug interactions --- migraine --- lasmiditan --- gepants --- monoclonal antibodies --- CYP1A1 --- CYP1A2 --- drug–drug interaction --- expression --- metabolism --- regulation --- drug transporter --- ubiquitination --- ixazomib --- DDI --- computational prediction --- in silico --- QSAR --- drug metabolism --- ADME --- CYP --- metabolic DDI --- P450 --- 1A2 --- 2B6 --- 2C19 --- 2C8 --- 2C9 --- 2D6 --- 3A4

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The aim of this Special Issue is to collect reports regarding all the recent strategies, directed at the improvement of antineoplastic activity of drugs in cancer progression, engaging all the expertise needed for the development of new anticancer drugs: medicinal chemistry, pharmacology, molecular biology, and computational and drug delivery studies.

Research & information: general --- Biology, life sciences --- EGR-1 --- flavonoid --- (E)-5-((4-oxo-4H-chromen-3-yl)methyleneamino)-1-phenyl-1H-pyrazole-4-carbonitrile --- MDA-MB-231 --- MMP9 --- TNFα --- pancreatic ductal adenocarcinoma --- cyclodextrin inclusion complex --- phase solubility studies --- preformulation studies --- biphenylnicotinamide derivatives --- dual inhibitor --- EGFR --- VEGFR2 --- ligand-based pharmacophore --- molecular docking --- molecular dynamics --- leukemias --- doxorubicin --- inflammation --- drug delivery --- tumor targeting --- elastin-like polypeptide --- cell penetrating peptide --- matrix metalloproteinase --- doxorubicin resistance --- photosensitizer delivery system --- PAMAM dendrimer --- photodynamic therapy --- cytotoxicity --- phototoxicity --- colorectal adenocarcinoma --- dicarboximides --- chemical synthesis --- apoptosis --- kinases --- anticancer --- gene profiling --- SAR --- biomarkers --- colorectal cancer --- early detection examination --- liquid biopsy --- personalized medicine --- tumor treatment --- exosomes --- ctDNA --- CTC --- cytotoxic activity --- pyrazole derivatives --- MTT assay --- ADMET analysis --- single-crystal diffraction --- FTIR spectroscopy --- NMR spectroscopy thermogravimetric analysis --- acute myelogenous leukemia --- platelets --- microparticles --- γδ T cells --- immunotherapy --- tumor resistance --- combination therapy --- tumor microenvironment --- immune checkpoint inhibitor --- neuroblastoma --- molecular iodine --- cyclophosphamide --- xenografts --- metronomic therapy --- tamoxifen --- CYP2D6 --- MCF-7 --- Ishikawa cells --- SERM --- TNBC --- uterotrophic --- α-mangostin --- poly(amidoamine) dendrimer --- targeted drug delivery --- biotin targeting --- glioblastoma multiforme --- squamous cell carcinoma --- antiparasitic therapy --- diclofenac --- indomethacin --- oleanolic acid derivative conjugates --- NF-κB --- Nrf2 --- MAPKs --- PSN-1 cells --- reactive oxygen species --- glioblastoma --- brain tumor --- extracellular vesicles --- pancreatic cancer --- paclitaxel --- clathrin --- endocytosis --- sulforaphane --- nicotine --- metalloproteinase-9 --- gastric cancer --- cell invasion --- Arylquin 1 --- colon cancer --- tumor progression --- azelastine --- oxidative stress --- autophagy --- mitotic catastrophe --- chronic myeloid leukemia --- imatinib --- tyrosine kinase --- ketoconazole --- P-glycoprotein --- drug efflux transporter --- non-small-cell lung cancer --- cisplatin resistance --- aldehyde dehydrogenase --- isothiocyanates --- disulfiram --- epithelial to mesenchymal transition --- aminopeptidase N --- acetamidophenones --- Schiff bases --- semicarbazones --- thiosemicarbazones --- inhibition of proliferation