Base de dados : MEDLINE
Pesquisa : D02.092.146.100 [Categoria DeCS]
Referências encontradas : 1341 [refinar]
Mostrando: 1 .. 10   no formato [Detalhado]

página 1 de 135 ir para página                         

  1 / 1341 MEDLINE  
              next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:29363539
[Au] Autor:Pirmohamed M
[Ad] Endereço:Department of Molecular and Clinical Pharmacology, Institute of Translational Medicine, University of Liverpool, Liverpool, UK.
[Ti] Título:Nucleic acid based therapies: developing frontier for precision medicine.
[So] Source:BMJ;360:k223, 2018 01 23.
[Is] ISSN:1756-1833
[Cp] País de publicação:England
[La] Idioma:eng
[Mh] Termos MeSH primário: Terapia Genética/utilização
Terapia de Alvo Molecular/utilização
Ácidos Nucleicos/uso terapêutico
Medicina de Precisão/métodos
[Mh] Termos MeSH secundário: Adenoviridae/genética
Aminofenóis/uso terapêutico
Agonistas dos Canais de Cloreto/uso terapêutico
Fibrose Cística/tratamento farmacológico
Fibrose Cística/genética
Regulador de Condutância Transmembrana em Fibrose Cística/efeitos dos fármacos
Regulador de Condutância Transmembrana em Fibrose Cística/genética
Terapia Genética/economia
Genômica
Hemofilia A/classificação
Hemofilia A/tratamento farmacológico
Hemofilia A/genética
Seres Humanos
Doença dos Neurônios Motores/tratamento farmacológico
Doença dos Neurônios Motores/genética
Mutação
Oligonucleotídeos Antissenso/economia
Oligonucleotídeos Antissenso/uso terapêutico
Quinolonas/uso terapêutico
Reino Unido/epidemiologia
[Pt] Tipo de publicação:EDITORIAL
[Nm] Nome de substância:
0 (Aminophenols); 0 (CFTR protein, human); 0 (Chloride Channel Agonists); 0 (Nucleic Acids); 0 (Oligonucleotides, Antisense); 0 (Quinolones); 126880-72-6 (Cystic Fibrosis Transmembrane Conductance Regulator); 1Y740ILL1Z (ivacaftor)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180305
[Lr] Data última revisão:
180305
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:180125
[St] Status:MEDLINE
[do] DOI:10.1136/bmj.k223


  2 / 1341 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:29183075
[Au] Autor:Van Wagoner RM; Eichner A; Bhasin S; Deuster PA; Eichner D
[Ad] Endereço:Sports Medicine Research and Testing Laboratory, Salt Lake City, Utah.
[Ti] Título:Chemical Composition and Labeling of Substances Marketed as Selective Androgen Receptor Modulators and Sold via the Internet.
[So] Source:JAMA;318(20):2004-2010, 2017 11 28.
[Is] ISSN:1538-3598
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Importance: Recent reports have described the increasing use of nonsteroidal selective androgen receptor modulators, which have not been approved by the US Food and Drug Administration (FDA), to enhance appearance and performance. The composition and purity of such products is not known. Objective: To determine the chemical identity and the amounts of ingredients in dietary supplements and products marketed and sold through the internet as selective androgen receptor modulators and compare the analyzed contents with product labels. Design and Setting: Web-based searches were performed from February 18, 2016, to March 25, 2016, using the Google search engine on the Chrome and Internet Explorer web browsers to identify suppliers selling selective androgen receptor modulators. The products were purchased and the identities of the compounds and their amounts were determined from April to August 2016 using chain-of-custody and World Anti-Doping Association-approved analytical procedures. Analytical findings were compared against the label information. Exposures: Products marketed and sold as selective androgen receptor modulators. Main Outcomes and Measures: Chemical identities and the amount of ingredients in each product marketed and sold as selective androgen receptor modulators. Results: Among 44 products marketed and sold as selective androgen receptor modulators, only 23 (52%) contained 1 or more selective androgen receptor modulators (Ostarine, LGD-4033, or Andarine). An additional 17 products (39%) contained another unapproved drug, including the growth hormone secretagogue ibutamoren, the peroxisome proliferator-activated receptor-δ agonist GW501516, and the Rev-ErbA agonist SR9009. Of the 44 tested products, no active compound was detected in 4 (9%) and substances not listed on the label were contained in 11 (25%). In only 18 of the 44 products (41%), the amount of active compound in the product matched that listed on the label. The amount of the compounds listed on the label differed substantially from that found by analysis in 26 of 44 products (59%). Conclusions and Relevance: In this limited investigation involving chemical analyses of 44 products marketed as selective androgen receptor modulators and sold via the internet, most products contained unapproved drugs and substances. Only 52% contained selective androgen receptor modulators and many were inaccurately labeled.
[Mh] Termos MeSH primário: Anabolizantes/química
Comércio
Rotulagem de Medicamentos
Internet
Substâncias para Melhoria do Desempenho/química
Receptores Androgênicos
[Mh] Termos MeSH secundário: Acetamidas/análise
Aminofenóis/análise
Anilidas/análise
Aprovação de Drogas
Tráfico de Drogas
Nitrilos/análise
Pirrolidinas/análise
Estados Unidos
United States Food and Drug Administration
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL
[Nm] Nome de substância:
0 (4-(2-(2,2,2-trifluoro-1-hydroxyethyl)pyrrolidin-1-yl)-2-(trifluoromethyl)benzonitrile); 0 (Acetamides); 0 (Aminophenols); 0 (Anabolic Agents); 0 (Anilides); 0 (Nitriles); 0 (Performance-Enhancing Substances); 0 (Pyrrolidines); 0 (Receptors, Androgen); 7UT2HAH49H (andarine); O3571H3R8N (ostarine)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:180228
[Lr] Data última revisão:
180228
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:171129
[St] Status:MEDLINE
[do] DOI:10.1001/jama.2017.17069


  3 / 1341 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28459323
[Au] Autor:Ramsey BW; Welsh MJ
[Ad] Endereço:1 Department of Pediatrics University of Washington School of Medicine Seattle, Washington.
[Ti] Título:AJRCCM: 100-Year Anniversary. Progress along the Pathway of Discovery Leading to Treatment and Cure of Cystic Fibrosis.
[So] Source:Am J Respir Crit Care Med;195(9):1092-1099, 2017 05 01.
[Is] ISSN:1535-4970
[Cp] País de publicação:United States
[La] Idioma:eng
[Mh] Termos MeSH primário: Aminofenóis/uso terapêutico
Aminopiridinas/uso terapêutico
Antibacterianos/uso terapêutico
Benzodioxóis/uso terapêutico
Agonistas dos Canais de Cloreto/uso terapêutico
Fibrose Cística/tratamento farmacológico
Publicações Periódicas como Assunto/história
Pneumologia/história
Quinolonas/uso terapêutico
[Mh] Termos MeSH secundário: Aniversários e Eventos Especiais
Fibrose Cística/genética
Fibrose Cística/história
Regulador de Condutância Transmembrana em Fibrose Cística/genética
Combinação de Medicamentos
Terapia de Reposição de Enzimas
História do Século XX
História do Século XXI
Mutação
[Pt] Tipo de publicação:HISTORICAL ARTICLE; JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Aminophenols); 0 (Aminopyridines); 0 (Anti-Bacterial Agents); 0 (Benzodioxoles); 0 (CFTR protein, human); 0 (Chloride Channel Agonists); 0 (Drug Combinations); 0 (Quinolones); 0 (lumacaftor, ivacaftor drug combination); 126880-72-6 (Cystic Fibrosis Transmembrane Conductance Regulator); 1Y740ILL1Z (ivacaftor)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:180214
[Lr] Data última revisão:
180214
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170502
[St] Status:MEDLINE
[do] DOI:10.1164/rccm.201702-0266ED


  4 / 1341 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:29241892
[Au] Autor:Dilokthornsakul P; Patidar M; Campbell JD
[Ad] Endereço:Center of Pharmaceutical Outcomes Research, Department of Pharmacy Practice, Faculty of Pharmaceutical Sciences, Naresuan University, Phitsanulok, Thailand. Electronic address: piyamethd@nu.ac.th.
[Ti] Título:Forecasting the Long-Term Clinical and Economic Outcomes of Lumacaftor/Ivacaftor in Cystic Fibrosis Patients with Homozygous phe508del Mutation.
[So] Source:Value Health;20(10):1329-1335, 2017 12.
[Is] ISSN:1524-4733
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:OBJECTIVES: To forecast lifetime outcomes and cost of lumacaftor/ivacaftor combination therapy in patients with cystic fibrosis (CF) with homozygous phe508del mutation from the US payer perspective. METHODS: A lifetime Markov model was developed from a US payer perspective. The model included five health states: 1) mild lung disease (percent predicted forced expiratory volume in 1 second [FEV ] >70%), 2) moderate lung disease (40% ≤ FEV ≤ 70%), 3) severe lung disease (FEV < 40%), 4) lung transplantation, and 5) death. All inputs were derived from published literature. We estimated lumacaftor/ivacaftor's improvement in outcomes compared with a non-CF referent population as well as CF-specific mortality estimates. RESULTS: Lumacaftor/ivacaftor was associated with additional 2.91 life-years (95% credible interval 2.55-3.56) and additional 2.42 quality-adjusted life-years (QALYs) (95% credible interval 2.10-2.98). Lumacaftor/ivacaftor was associated with improvements in survival and QALYs equivalent to 27.6% and 20.7%, respectively, for the survival and QALY gaps between CF usual care and their non-CF peers. The incremental lifetime cost was $2,632,249. CONCLUSIONS: Lumacaftor/ivacaftor increased life-years and QALYs in CF patients with the homozygous phe508del mutation and moved morbidity and mortality closer to that of their non-CF peers but it came with higher cost.
[Mh] Termos MeSH primário: Aminofenóis/administração & dosagem
Aminopiridinas/administração & dosagem
Benzodioxóis/administração & dosagem
Regulador de Condutância Transmembrana em Fibrose Cística/genética
Fibrose Cística/tratamento farmacológico
Anos de Vida Ajustados por Qualidade de Vida
Quinolonas/administração & dosagem
[Mh] Termos MeSH secundário: Adulto
Aminofenóis/economia
Aminopiridinas/economia
Benzodioxóis/economia
Fibrose Cística/genética
Fibrose Cística/fisiopatologia
Combinação de Medicamentos
Volume Expiratório Forçado
Homozigoto
Seres Humanos
Cadeias de Markov
Mutação
Quinolonas/economia
Índice de Gravidade de Doença
Resultado do Tratamento
Estados Unidos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Aminophenols); 0 (Aminopyridines); 0 (Benzodioxoles); 0 (Drug Combinations); 0 (Quinolones); 0 (cystic fibrosis transmembrane conductance regulator delta F508); 0 (lumacaftor, ivacaftor drug combination); 126880-72-6 (Cystic Fibrosis Transmembrane Conductance Regulator)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:180202
[Lr] Data última revisão:
180202
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171216
[St] Status:MEDLINE


  5 / 1341 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:27773592
[Au] Autor:Fidler MC; Beusmans J; Panorchan P; Van Goor F
[Ad] Endereço:Vertex Pharmaceuticals LLC, 11010 Torreyanna Road, San Diego, CA 92121,USA. Electronic address: Meredith_fidler@vrtx.com.
[Ti] Título:Correlation of sweat chloride and percent predicted FEV in cystic fibrosis patients treated with ivacaftor.
[So] Source:J Cyst Fibros;16(1):41-44, 2017 Jan.
[Is] ISSN:1873-5010
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Ivacaftor, a CFTR potentiator that enhances chloride transport by acting directly on CFTR to increase its channel gating activity, has been evaluated in patients with different CFTR mutations. Several previous analyses have reported no statistical correlation between change from baseline in ppFEV and reduction in sweat chloride levels for individuals treated with ivacaftor. The objective of the post hoc analysis described here was to expand upon previous analyses and evaluate the correlation between sweat chloride levels and absolute ppFEV changes across multiple cohorts of patients with different CF-causing mutations who were treated with ivacaftor. The goal of the analysis was to help define the potential value of sweat chloride as a pharmacodynamic biomarker for use in CFTR modulator trials. For any given study, reductions in sweat chloride levels and improvements in absolute ppFEV were not correlated for individual patients. However, when the data from all studies were combined, a statistically significant correlation between sweat chloride levels and ppFEV changes was observed (p<0.0001). Thus, sweat chloride level changes in response to potentiation of the CFTR protein by ivacaftor appear to be a predictive pharmacodynamic biomarker of lung function changes on a population basis but are unsuitable for the prediction of treatment benefits for individuals.
[Mh] Termos MeSH primário: Aminofenóis
Cloretos/análise
Regulador de Condutância Transmembrana em Fibrose Cística/genética
Volume Expiratório Forçado/efeitos dos fármacos
Quinolonas
Suor/química
[Mh] Termos MeSH secundário: Aminofenóis/administração & dosagem
Aminofenóis/farmacocinética
Biomarcadores/análise
Agonistas dos Canais de Cloreto/administração & dosagem
Agonistas dos Canais de Cloreto/farmacocinética
Ensaios Clínicos como Assunto
Fibrose Cística/diagnóstico
Fibrose Cística/tratamento farmacológico
Fibrose Cística/genética
Seres Humanos
Mutação
Valor Preditivo dos Testes
Quinolonas/administração & dosagem
Quinolonas/farmacocinética
Resultado do Tratamento
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Aminophenols); 0 (Biomarkers); 0 (Chloride Channel Agonists); 0 (Chlorides); 0 (Quinolones); 126880-72-6 (Cystic Fibrosis Transmembrane Conductance Regulator); 1Y740ILL1Z (ivacaftor)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180105
[Lr] Data última revisão:
180105
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161025
[St] Status:MEDLINE


  6 / 1341 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28465627
[Au] Autor:Falzone M; Crespo E; Jones K; Khan G; Korn VL; Patel A; Patel M; Patel K; Perkins C; Siddiqui S; Stenger D; Yu E; Gelber M; Scheffler R; Nayda V; Ravin A; Komal R; Rudolf JD; Shen B; Gullo V; Demain AL
[Ad] Endereço:Research Institute of Scientists Emeriti (RISE), Charles A. Dana Research Institute, Drew University, Madison, NJ, USA.
[Ti] Título:Nutritional control of antibiotic production by Streptomyces platensis MA7327: importance of l-aspartic acid.
[So] Source:J Antibiot (Tokyo);70(7):828-831, 2017 Jul.
[Is] ISSN:0021-8820
[Cp] País de publicação:Japan
[La] Idioma:eng
[Ab] Resumo:Streptomyces platensis MA7327 is a bacterium producing interesting antibiotics, which act by the novel mechanism of inhibiting fatty acid biosynthesis. The antibiotics produced by this actinomycete are platensimycin and platencin plus some minor related antibiotics. Platensimycin and platencin have activity against antibiotic-resistant bacteria such as methicillin-resistant Staphylococcus aureus and vancomycin-resistant Enterococcus; they also lack toxicity in animal models. Platensimycin also has activity against diabetes in a mouse model. We have been interested in studying the effects of primary metabolites on production of these antibiotics in our chemically defined production medium. In the present work, we tested 32 primary metabolites for their effect. They included 20 amino acids, 7 vitamins and 5 nucleic acid derivatives. Of these, only l-aspartic acid showed stimulation of antibiotic production. We conclude that the stimulatory effect of aspartic acid is due to its role as a precursor involved in the biosynthesis of aspartate-4-semialdehyde, which is the starting point for the biosynthesis of the 3-amino-2,4-dihydroxy benzoic acid portion of the platensimycin molecule.
[Mh] Termos MeSH primário: Antibacterianos/isolamento & purificação
Ácido Aspártico/administração & dosagem
Streptomyces/metabolismo
[Mh] Termos MeSH secundário: Adamantano/isolamento & purificação
Aminoácidos/administração & dosagem
Aminoácidos/metabolismo
Aminobenzoatos/isolamento & purificação
Aminofenóis/isolamento & purificação
Anilidas/isolamento & purificação
Antibacterianos/biossíntese
Ácido Aspártico/química
Ácidos Nucleicos/administração & dosagem
Ácidos Nucleicos/metabolismo
Compostos Policíclicos/isolamento & purificação
Vitaminas/administração & dosagem
Vitaminas/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Amino Acids); 0 (Aminobenzoates); 0 (Aminophenols); 0 (Anilides); 0 (Anti-Bacterial Agents); 0 (Nucleic Acids); 0 (Polycyclic Compounds); 0 (Vitamins); 0 (platencin); 30KYC7MIAI (Aspartic Acid); PJY633525U (Adamantane); Q3DQ78KOFY (platensimycin)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:180101
[Lr] Data última revisão:
180101
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170504
[St] Status:MEDLINE
[do] DOI:10.1038/ja.2017.49


  7 / 1341 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:29246444
[Au] Autor:Riquelme SA; Hopkins BD; Wolfe AL; DiMango E; Kitur K; Parsons R; Prince A
[Ad] Endereço:Department of Pediatrics, Columbia University, New York, NY 10032, USA.
[Ti] Título:Cystic Fibrosis Transmembrane Conductance Regulator Attaches Tumor Suppressor PTEN to the Membrane and Promotes Anti Pseudomonas aeruginosa Immunity.
[So] Source:Immunity;47(6):1169-1181.e7, 2017 Dec 19.
[Is] ISSN:1097-4180
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The tumor suppressor PTEN controls cell proliferation by regulating phosphatidylinositol-3-kinase (PI3K) activity, but the participation of PTEN in host defense against bacterial infection is less well understood. Anti-inflammatory PI3K-Akt signaling is suppressed in patients with cystic fibrosis (CF), a disease characterized by hyper-inflammatory responses to airway infection. We found that Ptenl mice, which lack the NH -amino terminal splice variant of PTEN, were unable to eradicate Pseudomonas aeruginosa from the airways and could not generate sufficient anti-inflammatory PI3K activity, similar to what is observed in CF. PTEN and the CF transmembrane conductance regulator (CFTR) interacted directly and this interaction was necessary to position PTEN at the membrane. CF patients under corrector-potentiator therapy, which enhances CFTR transport to the membrane, have increased PTEN amounts. These findings suggest that improved CFTR trafficking could enhance P. aeruginosa clearance from the CF airway by activating PTEN-mediated anti-bacterial responses and might represent a therapeutic strategy.
[Mh] Termos MeSH primário: Membrana Celular/imunologia
Regulador de Condutância Transmembrana em Fibrose Cística/imunologia
Fibrose Cística/imunologia
PTEN Fosfo-Hidrolase/imunologia
Infecções por Pseudomonas/imunologia
[Mh] Termos MeSH secundário: Aminofenóis/farmacologia
Aminopiridinas/farmacologia
Animais
Benzodioxóis/farmacologia
Membrana Celular/efeitos dos fármacos
Fibrose Cística/tratamento farmacológico
Fibrose Cística/genética
Fibrose Cística/microbiologia
Regulador de Condutância Transmembrana em Fibrose Cística/genética
Regulação da Expressão Gênica
Seres Humanos
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Knockout
Modelos Moleculares
Monócitos/efeitos dos fármacos
Monócitos/imunologia
Monócitos/microbiologia
PTEN Fosfo-Hidrolase/deficiência
PTEN Fosfo-Hidrolase/genética
Fosfatidilinositol 3-Quinases/genética
Fosfatidilinositol 3-Quinases/imunologia
Ligação Proteica
Conformação Proteica
Transporte Proteico
Proteínas Proto-Oncogênicas c-akt/genética
Proteínas Proto-Oncogênicas c-akt/imunologia
Infecções por Pseudomonas/genética
Infecções por Pseudomonas/microbiologia
Pseudomonas aeruginosa/imunologia
Quinolonas/farmacologia
Transdução de Sinais
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Aminophenols); 0 (Aminopyridines); 0 (Benzodioxoles); 0 (CFTR protein, human); 0 (Quinolones); 126880-72-6 (Cystic Fibrosis Transmembrane Conductance Regulator); 1Y740ILL1Z (ivacaftor); EC 2.7.1.- (Phosphatidylinositol 3-Kinases); EC 2.7.11.1 (Proto-Oncogene Proteins c-akt); EC 3.1.3.67 (PTEN Phosphohydrolase); EC 3.1.3.67 (PTEN protein, human); EC 3.1.3.67 (Pten protein, mouse); EGP8L81APK (lumacaftor)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:171226
[Lr] Data última revisão:
171226
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171217
[St] Status:MEDLINE


  8 / 1341 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:29209709
[Au] Autor:Cutting GR
[Ad] Endereço:McKusick Nathans Institute of Genetic Medicine, Johns Hopkins University School of Medicine, Baltimore, Maryland.
[Ti] Título:Treating Specific Variants Causing Cystic Fibrosis.
[So] Source:JAMA;318(21):2130-2131, 2017 12 05.
[Is] ISSN:1538-3598
[Cp] País de publicação:United States
[La] Idioma:eng
[Mh] Termos MeSH primário: Aminofenóis/uso terapêutico
Aminopiridinas/uso terapêutico
Benzodioxóis/uso terapêutico
Agonistas dos Canais de Cloreto/uso terapêutico
Regulador de Condutância Transmembrana em Fibrose Cística/genética
Fibrose Cística/tratamento farmacológico
Quinolonas/uso terapêutico
[Mh] Termos MeSH secundário: Fibrose Cística/genética
Combinação de Medicamentos
Variação Genética
Seres Humanos
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Aminophenols); 0 (Aminopyridines); 0 (Benzodioxoles); 0 (CFTR protein, human); 0 (Chloride Channel Agonists); 0 (Drug Combinations); 0 (Quinolones); 0 (lumacaftor, ivacaftor drug combination); 126880-72-6 (Cystic Fibrosis Transmembrane Conductance Regulator); 1Y740ILL1Z (ivacaftor)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:171219
[Lr] Data última revisão:
171219
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:171207
[St] Status:MEDLINE
[do] DOI:10.1001/jama.2017.16823


  9 / 1341 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28927789
[Au] Autor:Takahashi N; Koyama S; Hasegawa S; Yamasaki M; Imai M
[Ad] Endereço:Laboratory of Physiological Chemistry, Institute of Medicinal Chemistry, Hoshi University, 2-4-41 Ebara, Shinagawa, Tokyo 142-8501, Japan. Electronic address: t-noriko@hoshi.ac.jp.
[Ti] Título:Anticancer efficacy of p-dodecylaminophenol against high-risk and refractory neuroblastoma cells in vitro and in vivo.
[So] Source:Bioorg Med Chem Lett;27(20):4664-4672, 2017 10 15.
[Is] ISSN:1464-3405
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Neuroblastoma is an aggressive and drug-resistant refractory cancer. The human high-risk neuroblastoma cell line, SK-N-AS (non-amplified N-myc) is derived from stromal cells and it is resistant to treatment with retinoic acid (1, RA), which is a chemotherapeutic agent used to induce neuronal cellular differentiation of neuroblastomas. We have developed p-dodecylaminophenol (3, p-DDAP), based on N-(4-hydroxyphenyl)retinamide (2, 4-HPR), a synthetic amide of 1, since 1 and 2 are associated with the side-effect of nyctalopia. In order to evaluate the effects of 3 on high-risk neuroblastomas, we employed SK-N-AS cells as well asa second high-risk human neuroblastoma cell line, IMR-32, which is derived from neuronal cells (amplified N-myc, drug sensitive). Compound 3 suppressed cell growth of SK-N-AS and IMR-32 cells more effectively than 1, 2, p-decylaminophenol (4, p-DAP), N-(4-hydroxyphenyl)dodecananamide (5, 4-HPDD) or N-(4-hydroxyphenyl)decananamide (6, 4-HPD). In SK-N-AS cells, 3 induced G /G arrest and apoptosis to a greater extent than 1 and 2. In IMR-32 cells, 3 induced apoptosis to a similar extent as 1 and 2, potentially by inhibiting N-myc expression. In addition, i.p. administration of 3 suppressed tumor growth in SK-N-AS-implanted mice in vivo. Since 3 showed no effects on blood retinol concentrations, in contrast to reductions following the administration of 2, it exhibited excellent anticancer efficacy against high-risk neuroblastoma SK-N-AS and IMR-32 expressing distinct levels of N-myc. Compound 3 may have potential for clinical use in the treatment of refractory neuroblastoma with reduced side effects.
[Mh] Termos MeSH primário: Aminofenóis/química
Aminofenóis/farmacologia
Antineoplásicos/química
Antineoplásicos/farmacologia
Apoptose/efeitos dos fármacos
[Mh] Termos MeSH secundário: Aminofenóis/uso terapêutico
Animais
Antineoplásicos/uso terapêutico
Caspase 3/metabolismo
Linhagem Celular Tumoral
Pontos de Checagem da Fase G1 do Ciclo Celular/efeitos dos fármacos
Regulação Neoplásica da Expressão Gênica/efeitos dos fármacos
Seres Humanos
Masculino
Camundongos
Camundongos Nus
Proteína Proto-Oncogênica N-Myc/genética
Proteína Proto-Oncogênica N-Myc/metabolismo
Neuroblastoma/tratamento farmacológico
Neuroblastoma/metabolismo
Neuroblastoma/patologia
Proteínas Proto-Oncogênicas c-bcl-2/genética
Proteínas Proto-Oncogênicas c-bcl-2/metabolismo
Transplante Heterólogo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (4-dodecylaminophenol); 0 (Aminophenols); 0 (Antineoplastic Agents); 0 (N-Myc Proto-Oncogene Protein); 0 (Proto-Oncogene Proteins c-bcl-2); EC 3.4.22.- (Caspase 3)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171125
[Lr] Data última revisão:
171125
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170921
[St] Status:MEDLINE


  10 / 1341 MEDLINE  
              first record previous record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28891346
[Au] Autor:Bulloch MN; Hanna C; Giovane R
[Ad] Endereço:a Harrison School of Pharmacy , Auburn University , Auburn , AL , USA.
[Ti] Título:Lumacaftor/ivacaftor, a novel agent for the treatment of cystic fibrosis patients who are homozygous for the F580del CFTR mutation.
[So] Source:Expert Rev Clin Pharmacol;10(10):1055-1072, 2017 Oct.
[Is] ISSN:1751-2441
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:INTRODUCTION: Cystic Fibrosis (CF) is an autosomal recessive disease affecting up to 90,000 people worldwide. Approximately 73% of patients are homozygous for the F508del cystic fibrosis transmembrane conductance regulator [CFTR] mutation. Traditionally treatment has only included supportive care. Therefore, there is a need for safe and effective novel therapies targeting the underlying molecular defects seen with CF. Areas covered: In 2016, the Food and Drug Administration and the European Commission approved LUM/IVA (Orkambi), a CFTR modulator that includes both a CFTR corrector and potentiator, for CF patients homozygous for the F508del CFTR mutation. This article reviews the pharmacologic features, clinical efficacy, and safety of LUM/IVA and summarize the available pre-clinical and clinical data of LUM/IVA use. Expert commentary: LUM/IVA showed modest, but significant improvements from baseline in percent predicted FEV (ppFEV ) as well as a reduction in pulmonary exacerbations by 35% It was shown to be safe for short- and long-term use. Currently, LUM/IVA is the only oral agent in its class available and represents a milestone the development of therapies for the management of CF. Nonetheless, pharmacoeconomic data are necessary to justify its high cost before is use becomes standard of care.
[Mh] Termos MeSH primário: Aminofenóis/uso terapêutico
Aminopiridinas/uso terapêutico
Benzodioxóis/uso terapêutico
Regulador de Condutância Transmembrana em Fibrose Cística/genética
Fibrose Cística/tratamento farmacológico
Quinolonas/uso terapêutico
[Mh] Termos MeSH secundário: Aminofenóis/efeitos adversos
Aminofenóis/farmacologia
Aminopiridinas/efeitos adversos
Aminopiridinas/farmacologia
Animais
Benzodioxóis/efeitos adversos
Benzodioxóis/farmacologia
Fibrose Cística/genética
Fibrose Cística/fisiopatologia
Combinação de Medicamentos
Volume Expiratório Forçado
Seres Humanos
Terapia de Alvo Molecular
Mutação
Quinolonas/efeitos adversos
Quinolonas/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Aminophenols); 0 (Aminopyridines); 0 (Benzodioxoles); 0 (Drug Combinations); 0 (Quinolones); 0 (lumacaftor, ivacaftor drug combination); 126880-72-6 (Cystic Fibrosis Transmembrane Conductance Regulator)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171013
[Lr] Data última revisão:
171013
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170912
[St] Status:MEDLINE
[do] DOI:10.1080/17512433.2017.1378094



página 1 de 135 ir para página                         
   


Refinar a pesquisa
  Base de dados : MEDLINE Formulário avançado   

    Pesquisar no campo  
1  
2
3
 
           



Search engine: iAH v2.6 powered by WWWISIS

BIREME/OPAS/OMS - Centro Latino-Americano e do Caribe de Informação em Ciências da Saúde