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[PMID]:28630284
[Au] Autor:Burckhardt BC; Henjakovic M; Hagos Y; Burckhardt G
[Ad] Endereço:Center of Physiology and Pathophysiology, University Medical Center Goettingen, Goettingen, Germany (B.C.B, M.H., Y.H., G.B.); Department I of Internal Medicine, University Medical Center Cologne, Cologne, Germany (M.H.); and PortaCellTec Biosciences GmbH, Goettingen, Germany (Y.H.) birgitta.burckha
[Ti] Título:Differential Interaction of Dantrolene, Glafenine, Nalidixic Acid, and Prazosin with Human Organic Anion Transporters 1 and 3.
[So] Source:J Pharmacol Exp Ther;362(3):450-458, 2017 Sep.
[Is] ISSN:1521-0103
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:In renal proximal tubule cells, the organic anion transporters 1 and 3 (OAT1 and OAT3) in the basolateral membrane and the multidrug resistance-associated protein 4 (MRP4) in the apical membrane share substrates and co-operate in renal drug secretion. We hypothesized that recently identified MRP4 inhibitors dantrolene, glafenine, nalidixic acid, and prazosin also interact with human OAT1 and/or OAT3 stably transfected in human embryonic kidney 293 cells. These four drugs were tested as possible inhibitors of -[ H]aminohippurate (PAH) and [ C]glutarate uptake by OAT1, and of [ H]estrone-3-sulfate (ES) uptake by OAT3. In addition, we explored whether these drugs decrease the equilibrium distribution of radiolabeled PAH, glutarate, or ES, an approach intended to indirectly suggest drug/substrate exchange through OAT1 and OAT3. With OAT3, a dose-dependent inhibition of [ H]ES uptake and a downward shift in [ H]ES equilibrium were observed, indicating that all four drugs bind to OAT3 and may possibly be translocated. In contrast, the interaction with OAT1 was more complex. With [ C]glutarate as substrate, all four drugs inhibited uptake but only glafenine and nalidixic acid shifted glutarate equilibrium. Using [ H]PAH as a substrate of OAT1, nalidixic acid inhibited but dantrolene, glafenine, and prazosin stimulated uptake. Nalidixic acid decreased equilibrium content of [ H]PAH, suggesting that it may possibly be exchanged by OAT1. Taken together, OAT1 and OAT3 interact with the MRP4 inhibitors dantrolene, glafenine, nalidixic acid, and prazosin, indicating overlapping specificities. At OAT1, more than one binding site must be assumed to explain substrate and drug-dependent stimulation and inhibition of transport activity.
[Mh] Termos MeSH primário: Dantroleno/metabolismo
Glafenina/metabolismo
Ácido Nalidíxico/metabolismo
Proteína 1 Transportadora de Ânions Orgânicos/metabolismo
Transportadores de Ânions Orgânicos Sódio-Independentes/metabolismo
Prazosina/metabolismo
[Mh] Termos MeSH secundário: Ligação Competitiva
Técnicas de Cultura de Células
Estrona/análogos & derivados
Estrona/metabolismo
Células HEK293
Seres Humanos
Taxa de Depuração Metabólica
Proteína 1 Transportadora de Ânions Orgânicos/genética
Transportadores de Ânions Orgânicos Sódio-Independentes/genética
Ligação Proteica
Ensaio Radioligante
Eliminação Renal
Especificidade por Substrato
Transfecção
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Organic Anion Transport Protein 1); 0 (Organic Anion Transporters, Sodium-Independent); 0 (organic anion transport protein 3); 2DI9HA706A (Estrone); 3B91HWA56M (Nalidixic Acid); 46HL4I09AH (Glafenine); F64QU97QCR (Dantrolene); QTL48N278K (estrone sulfate); XM03YJ541D (Prazosin)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170817
[Lr] Data última revisão:
170817
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170621
[St] Status:MEDLINE
[do] DOI:10.1124/jpet.117.241406


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[PMID]:27160382
[Au] Autor:Sen S; An H; Menezes P; Oakes J; Eron J; Lin W; Robertson K; Powers W
[Ad] Endereço:Department of Neurology, University of South Carolina, Columbia, South Carolina. Electronic address: Souvik.Sen@uscmed.sc.edu.
[Ti] Título:Increased Cortical Cerebral Blood Flow in Asymptomatic Human Immunodeficiency Virus-Infected Subjects.
[So] Source:J Stroke Cerebrovasc Dis;25(8):1891-5, 2016 Aug.
[Is] ISSN:1532-8511
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Human immunodeficiency virus (HIV)-infected individuals are at high risk for ischemic stroke. To investigate the physiological basis for this risk, we used magnetic resonance imaging (MRI) to measure oxygen extraction fraction (OEF) and cerebral blood flow (CBF) in treatment-naive asymptomatic HIV-infected subjects and controls. METHODS: In treatment-naive asymptomatic HIV-infected subjects and age-, gender-, and race-matched controls, OEF was measured by MRI asymmetric spin-echo echo-planar imaging sequences and CBF was measured by MRI pseudocontinuous arterial spin labeling. RESULTS: Twenty-six treatment-naive HIV-infected subjects and 27 age-, gender-, race-matched controls participated. Whole-brain, gray matter (GM), and white matter OEF were not different between the groups (all P > .70). Unexpectedly, HIV-infected subjects had significantly higher CBF in cortical GM (72.9 ± 16.2 mL/100 g/min versus 63.9 ± 9.9 mL/100 g/min; P = .01) but not in subcortical GM (P = .25). CONCLUSIONS: The observed increase in cortical GM CBF in treatment-naive HIV-infected subjects is unexpected, contrary to CBF decreases reported in HIV-infected subjects on treatment, and may represent an initial increase in metabolic activity due to an HIV-mediated inflammation.
[Mh] Termos MeSH primário: Córtex Cerebral/patologia
Circulação Cerebrovascular/fisiologia
Infecções por HIV/patologia
[Mh] Termos MeSH secundário: Adulto
Antirretrovirais/uso terapêutico
Estudos de Casos e Controles
Córtex Cerebral/diagnóstico por imagem
Córtex Cerebral/virologia
Feminino
Glafenina/administração & dosagem
Glafenina/análogos & derivados
Infecções por HIV/diagnóstico por imagem
Infecções por HIV/tratamento farmacológico
Seres Humanos
Processamento de Imagem Assistida por Computador
Imagem por Ressonância Magnética
Masculino
Estudos Retrospectivos
Marcadores de Spin
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anti-Retroviral Agents); 0 (Spin Labels); 46HL4I09AH (Glafenine); F1DZD948G6 (nicafenine)
[Em] Mês de entrada:1704
[Cu] Atualização por classe:170801
[Lr] Data última revisão:
170801
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160511
[St] Status:MEDLINE


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[PMID]:26641551
[Au] Autor:Chiu AM; Mandziuk JJ; Loganathan SK; Alka K; Casey JR
[Ad] Endereço:Department of Physiology, University of Alberta, Edmonton, Alberta, Canada.
[Ti] Título:High Throughput Assay Identifies Glafenine as a Corrector for the Folding Defect in Corneal Dystrophy-Causing Mutants of SLC4A11.
[So] Source:Invest Ophthalmol Vis Sci;56(13):7739-53, 2015 Dec.
[Is] ISSN:1552-5783
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:PURPOSE: Protein misfolding, causing retention of nascent protein in the endoplasmic reticulum (ER), is the most common molecular phenotype for disease alleles of membrane proteins. Strategies are needed to identify therapeutics able to correct such folding/trafficking defects. Mutations of SLC4A11, a plasma membrane transport protein of the human corneal endothelial cell layer, cause cases of congenital hereditary endothelial dystrophy, Harboyan syndrome, and Fuchs' endothelial corneal dystrophy. Most SLC4A11 mutations induce SLC4A11 misfolding and retention in the ER. METHODS: An assay amenable to high-throughput screening was developed to quantify SLC4A11 at the plasma membrane, enabling a search for potential traffic-correcting small molecules. The assay was validated by comparing cell surface abundance of SLC4A11 mutants measured in the assay to observations from confocal immunofluorescence and values from cell surface biotinylation. Functionality of mutant proteins was assessed, using a confocal microscopic green fluorescent protein (GFP) water flux assay where relative rates of cell swelling are compared. RESULTS: A small-scale screen revealed that the nonsteroidal anti-inflammatory drugs (NSAIDs), glafenine, ibuprofen, and acetylsalicylic acid dissolved in 0.2% dimethyl sulfoxide (DMSO), partially rescued the trafficking defect in some SLC4A11 mutants, expressed in HEK293 cells. These SLC4A11 mutants retained functional activity when rescued to the plasma membrane by glafenine treatment. Glafenine was effective with an EC50 of 1.5 ± 0.7 µM. CONCLUSIONS: These data suggest that glafenine, and perhaps other NSAIDs, hold potential as therapeutics for misfolded membrane proteins, like SLC4A11. The high throughput approach described here can be modified to identify correctors of other misfolded plasma membrane proteins that cause eye disease.
[Mh] Termos MeSH primário: Analgésicos não Entorpecentes/farmacologia
Proteínas de Transporte de Ânions/metabolismo
Antiporters/metabolismo
Distrofias Hereditárias da Córnea/metabolismo
Glafenina/farmacologia
Mutação de Sentido Incorreto/efeitos dos fármacos
Dobramento de Proteína/efeitos dos fármacos
[Mh] Termos MeSH secundário: Proteínas de Transporte de Ânions/genética
Antiporters/genética
Linhagem Celular
Distrofias Hereditárias da Córnea/tratamento farmacológico
Distrofias Hereditárias da Córnea/genética
Células HEK293/efeitos dos fármacos
Células HEK293/metabolismo
Perda Auditiva Neurossensorial/metabolismo
Seres Humanos
Transporte Proteico/efeitos dos fármacos
Transporte Proteico/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T; VALIDATION STUDIES
[Nm] Nome de substância:
0 (Analgesics, Non-Narcotic); 0 (Anion Transport Proteins); 0 (Antiporters); 0 (SLC4A11 protein, human); 46HL4I09AH (Glafenine)
[Em] Mês de entrada:1605
[Cu] Atualização por classe:151208
[Lr] Data última revisão:
151208
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:151208
[St] Status:MEDLINE
[do] DOI:10.1167/iovs.15-17802


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[PMID]:22917923
[Au] Autor:Goldsmith JR; Cocchiaro JL; Rawls JF; Jobin C
[Ad] Endereço:Department of Pharmacology, University of North Carolina, Chapel Hill, NC 27599, USA.
[Ti] Título:Glafenine-induced intestinal injury in zebrafish is ameliorated by µ-opioid signaling via enhancement of Atf6-dependent cellular stress responses.
[So] Source:Dis Model Mech;6(1):146-59, 2013 Jan.
[Is] ISSN:1754-8411
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Beside their analgesic properties, opiates exert beneficial effects on the intestinal wound healing response. In this study, we investigated the role of µ-opioid receptor (MOR) signaling on the unfolded protein response (UPR) using a novel zebrafish model of NSAID-induced intestinal injury. The NSAID glafenine was administered to zebrafish larvae at 5 days post-fertilization (dpf) for up to 24 hours in the presence or absence of the MOR-specific agonist DALDA. By analysis with histology, transmission electron microscopy and vital dye staining, glafenine-treated zebrafish showed evidence of endoplasmic reticulum and mitochondrial stress, with disrupted intestinal architecture and halted cell stress responses, alongside accumulation of apoptotic intestinal epithelial cells in the lumen. Although the early UPR marker BiP was induced with glafenine-induced injury, downstream atf6 and s-xbp1 expression were paradoxically not increased, explaining the halted cell stress responses. The µ-opioid agonist DALDA protected against glafenine-induced injury through induction of atf6-dependent UPR. Our findings show that DALDA prevents glafenine-induced epithelial damage through induction of effective UPR.
[Mh] Termos MeSH primário: Fator 6 Ativador da Transcrição/metabolismo
Anti-Inflamatórios não Esteroides/toxicidade
Glafenina/toxicidade
Intestinos/efeitos dos fármacos
Intestinos/lesões
Receptores Opioides mu/metabolismo
Proteínas de Peixe-Zebra/metabolismo
[Mh] Termos MeSH secundário: Animais
Apoptose/efeitos dos fármacos
Modelos Animais de Doenças
Proteínas de Choque Térmico/metabolismo
Mucosa Intestinal/efeitos dos fármacos
Mucosa Intestinal/lesões
Mucosa Intestinal/metabolismo
Mucosa Intestinal/patologia
Intestinos/metabolismo
Intestinos/patologia
Oligopeptídeos/farmacologia
Receptores Opioides mu/agonistas
Transdução de Sinais/efeitos dos fármacos
Estresse Fisiológico
Resposta a Proteínas não Dobradas/efeitos dos fármacos
Peixe-Zebra
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL
[Nm] Nome de substância:
0 (Activating Transcription Factor 6); 0 (Anti-Inflammatory Agents, Non-Steroidal); 0 (Heat-Shock Proteins); 0 (Oligopeptides); 0 (Receptors, Opioid, mu); 0 (Zebrafish Proteins); 0 (molecular chaperone GRP78); 118476-85-0 (tyrosyl-arginyl-phenylalanyl-lysinamide); 46HL4I09AH (Glafenine)
[Em] Mês de entrada:1306
[Cu] Atualização por classe:170220
[Lr] Data última revisão:
170220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:120825
[St] Status:MEDLINE
[do] DOI:10.1242/dmm.009852


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[PMID]:21628497
[Au] Autor:Wen B; Moore DJ
[Ad] Endereço:Drug Metabolism, eADME, Non-Clinical Safety, Hoffmann-La Roche, Inc., 340 Kingsland Street, 123/1341, Nutley, NJ 07110, USA. bo.wen@roche.com
[Ti] Título:Bioactivation of glafenine by human liver microsomes and peroxidases: identification of electrophilic iminoquinone species and GSH conjugates.
[So] Source:Drug Metab Dispos;39(9):1511-21, 2011 Sep.
[Is] ISSN:1521-009X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Glafenine (Privadol; 2,3-dihydroxypropyl 2-[(7-chloro-4-quinolinyl) amino]benzoate) is a non-narcotic analgesic agent widely used for the treatment of pains of various origins. Severe liver toxicity and a high incidence of anaphylaxis were reported in patients treated with glafenine, eventually leading to its withdrawal from the market in most countries. It is proposed that bioactivation of glafenine and subsequent binding of reactive metabolite(s) to critical cellular proteins play a causative role. The study described herein aimed at characterizing pathways of glafenine bioactivation and the metabolic enzymes involved. Two GSH conjugates of glafenine were detected in human liver microsomal incubations using liquid chromatography tandem mass spectrometry. The structures of detected conjugates were determined as GSH adducts of 5-hydroxyglafenine (M3) and 5-hydroxy glafenic acid (M4), respectively. GSH conjugation took place with a strong preference at C6 of the benzene ring of glafenine, ortho to the carbonyl moiety. These findings are consistent with a bioactivation sequence involving initial cytochrome P450-catalyzed 5-hydroxylation of the benzene ring of glafenine, followed by two electron oxidations of M3 and M4 to form corresponding para-quinone imine intermediates that react with GSH to form GSH adducts M1 and M2, respectively. Formation of M1 and M2 was primarily catalyzed by heterologously expressed recombinant CYP3A4 and to a lesser extent, CYP2C19 and CYP2D6. We demonstrated that M3 can also be bioactivated by peroxidases, such as horseradish peroxidase and myeloperoxidase. In summary, these findings have significance in understanding the bioactivation pathways of glafenine and their potential link to mechanisms of toxicity of glafenine.
[Mh] Termos MeSH primário: Glafenina/química
Glafenina/metabolismo
Glutationa/química
Microssomos Hepáticos/enzimologia
Microssomos Hepáticos/metabolismo
Peroxidases/metabolismo
Quinonas/metabolismo
[Mh] Termos MeSH secundário: Ciclofilinas/metabolismo
Sistema Enzimático do Citocromo P-450/metabolismo
Glafenina/efeitos adversos
Seres Humanos
Inativação Metabólica
Microssomos Hepáticos/química
Oxirredução
Ligação Proteica
Espectrometria de Massas em Tandem/métodos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Quinones); 0 (iminoquinone); 46HL4I09AH (Glafenine); 9035-51-2 (Cytochrome P-450 Enzyme System); EC 1.11.1.- (Peroxidases); EC 5.2.1.- (Cyclophilins); EC 5.2.1.8 (PPIG protein, human); GAN16C9B8O (Glutathione)
[Em] Mês de entrada:1202
[Cu] Atualização por classe:141120
[Lr] Data última revisão:
141120
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:110602
[St] Status:MEDLINE
[do] DOI:10.1124/dmd.111.039396


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[PMID]:21223643
[Au] Autor:Walash M; Belal F; Eid M; el-Abass SA
[Ad] Endereço:Department of Analytical Chemistry, Faculty of Pharmacy, Mansoura University, Mansoura, 35516, Egypt.
[Ti] Título:Simultaneous HPLC determination of thiocolchicoside and glafenine as well as thiocolchicoside and floctafenine in their combined dosage forms.
[So] Source:J Chromatogr Sci;49(2):159-64, 2011 Feb.
[Is] ISSN:1945-239X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Sensitive and accurate high-performance liquid chromatographic methods have been developed for the simultaneous determination of thiocolchicoside (TC)-glafenine (GF) (Mix I) and thiocolchicoside-floctafenine (FN) (Mix II) in their pharmaceutical formulations. The analysis for both mixtures was performed using 250 mm × 4.6 mm i.d., 5 µm particle size C18 Waters Symmetry column. The mobile phase consisted of methanol-0.035 M phosphate buffer (50:50, v/v) of pH 4.5 for Mix I and methanol-0.03 M phosphate buffer (70:30, v/v) of pH 4 for Mix II with flow rate of 1 mL/min and UV detection at 400 nm in both cases. The calibration plots were rectilinear over the concentration range of 0.2-2 µg/mL for TC in both mixtures and 20-200 µg/mL for each of GF and FN . The limits of detection for TC and GF were 0.05 µg/mL and 0.62 µg/mL, respectively, and for TC and FN were 0.02 µg/mL and 0.70 µg/mL, respectively. Additionally, the proposed methods were successfully applied to their combined tablets with average percentage recoveries of 100.35 ± 0.61 and 100.57 ± 0.72% for TC and GF respectively and for TC and FN the percentage recoveries were 101.2 ± 0.72 and 100.36 ± 0.67%, respectively. The results obtained were favorably compared with those given using the comparison methods.
[Mh] Termos MeSH primário: Cromatografia Líquida de Alta Pressão/métodos
Colchicina/análogos & derivados
Glafenina/análise
ortoaminobenzoatos/análise
[Mh] Termos MeSH secundário: Calibragem
Química Farmacêutica
Colchicina/análise
Colchicina/química
Colchicina/isolamento & purificação
Combinação de Medicamentos
Glafenina/química
Glafenina/isolamento & purificação
Concentração de Íons de Hidrogênio
Modelos Lineares
Metanol
Reprodutibilidade dos Testes
Sensibilidade e Especificidade
ortoaminobenzoatos/química
ortoaminobenzoatos/isolamento & purificação
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Drug Combinations); 0 (ortho-Aminobenzoates); 46HL4I09AH (Glafenine); O04HVX6A9Q (floctafenine); SML2Y3J35T (Colchicine); T1X8S697GT (thiocolchicoside); Y4S76JWI15 (Methanol)
[Em] Mês de entrada:1104
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:110113
[St] Status:MEDLINE


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[PMID]:20200141
[Au] Autor:Robert R; Carlile GW; Liao J; Balghi H; Lesimple P; Liu N; Kus B; Rotin D; Wilke M; de Jonge HR; Scholte BJ; Thomas DY; Hanrahan JW
[Ad] Endereço:Physiology Department, McGill University, Montreal, Quebec, H3G 1Y6, Canada.
[Ti] Título:Correction of the Delta phe508 cystic fibrosis transmembrane conductance regulator trafficking defect by the bioavailable compound glafenine.
[So] Source:Mol Pharmacol;77(6):922-30, 2010 Jun.
[Is] ISSN:1521-0111
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Cystic fibrosis (CF) is caused by mutations in the CF transmembrane conductance regulator (CFTR) gene, which encodes a cAMP-activated anion channel expressed in epithelial cells. The most common mutation Delta Phe508 leads to protein misfolding, retention by the endoplasmic reticulum, and degradation. One promising therapeutic approach is to identify drugs that have been developed for other indications but that also correct the CFTR trafficking defect, thereby exploiting their known safety and bioavailability in humans and reducing the time required for clinical development. We have screened approved, marketed, and off-patent drugs with known safety and bioavailability using a Delta Phe508-CFTR trafficking assay. Among the confirmed hits was glafenine, an anthranilic acid derivative with analgesic properties. Its ability to correct the misprocessing of CFTR was confirmed by in vitro and in vivo studies using a concentration that is achieved clinically in plasma (10 microM). Glafenine increased the surface expression of Delta Phe508-CFTR in baby hamster kidney (BHK) cells to approximately 40% of that observed for wild-type CFTR, comparable with the known CFTR corrector 4-cyclohexyloxy-2-{1-[4-(4-methoxybenzensulfonyl)-piperazin-1-yl]-ethyl}-quinazoline (VRT-325). Partial correction was confirmed by the appearance of mature CFTR in Western blots and by two assays of halide permeability in unpolarized BHK and human embryonic kidney cells. Incubating polarized CFBE41o(-) monolayers and intestines isolated from Delta Phe508-CFTR mice (treated ex vivo) with glafenine increased the short-circuit current (I(sc)) response to forskolin + genistein, and this effect was abolished by 10 microM CFTR(inh)172. In vivo treatment with glafenine also partially restored total salivary secretion. We conclude that the discovery of glafenine as a CFTR corrector validates the approach of investigating existing drugs for the treatment of CF, although localized delivery or further medicinal chemistry may be needed to reduce side effects.
[Mh] Termos MeSH primário: Analgésicos não Entorpecentes/farmacocinética
Regulador de Condutância Transmembrana em Fibrose Cística/metabolismo
Glafenina/farmacocinética
Fenilalanina/genética
[Mh] Termos MeSH secundário: Animais
Disponibilidade Biológica
Western Blotting
Linhagem Celular
Cricetinae
Regulador de Condutância Transmembrana em Fibrose Cística/genética
Seres Humanos
Piperazinas/farmacologia
Transporte Proteico
Quinazolinas/farmacologia
Espectrometria de Fluorescência
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (4-cyclohexyloxy-2-(1-(4-(4-methoxy-benzenesulfonyl)piperazin-1-yl)ethyl)quinazoline); 0 (Analgesics, Non-Narcotic); 0 (Piperazines); 0 (Quinazolines); 126880-72-6 (Cystic Fibrosis Transmembrane Conductance Regulator); 46HL4I09AH (Glafenine); 47E5O17Y3R (Phenylalanine)
[Em] Mês de entrada:1006
[Cu] Atualização por classe:131121
[Lr] Data última revisão:
131121
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:100305
[St] Status:MEDLINE
[do] DOI:10.1124/mol.109.062679


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[PMID]:19567678
[Au] Autor:Zhang Y; Byun Y; Ren YR; Liu JO; Laterra J; Pomper MG
[Ad] Endereço:Russell H. Morgan Department of Radiology and Radiological Sciences, Johns Hopkins School of Medicine, Baltimore, Maryland, USA.
[Ti] Título:Identification of inhibitors of ABCG2 by a bioluminescence imaging-based high-throughput assay.
[So] Source:Cancer Res;69(14):5867-75, 2009 Jul 15.
[Is] ISSN:1538-7445
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:ABCG2 is a member of the ATP-binding cassette (ABC) family of transporters, the overexpression of which is associated with tumor resistance to a variety of chemotherapeutic agents. Accordingly, combining ABCG2 inhibitor(s) with chemotherapy has the potential to improve treatment outcome. To search for clinically useful ABCG2 inhibitors, a bioluminescence imaging (BLI)-based assay was developed to allow high-throughput compound screening. This assay exploits our finding that d-luciferin, the substrate of firefly luciferase (fLuc), is a specific substrate of ABCG2, and ABCG2 inhibitors block the export of d-luciferin and enhance bioluminescence signal by increasing intracellular d-luciferin concentrations. HEK293 cells, engineered to express ABCG2 and fLuc, were used to screen the Hopkins Drug Library that includes drugs approved by the Food and Drug Administration (FDA) as well as drug candidates that have entered phase II clinical trials. Forty-seven compounds showed BLI enhancement, a measure of anti-ABCG2 activity, of > or =5-fold, the majority of which were not previously known as ABCG2 inhibitors. The assay was validated by its identification of known ABCG2 inhibitors and by confirming previously unknown ABCG2 inhibitors using established in vitro assays (e.g., mitoxantrone resensitization and BODIPY-prazosin assays). Glafenine, a potent new inhibitor, also inhibited ABCG2 activity in vivo. The BLI-based assay is an efficient method to identify new inhibitors of ABCG2. As they were derived from a FDA-approved compound library, many of the inhibitors uncovered in this study are ready for clinical testing.
[Mh] Termos MeSH primário: Transportadores de Cassetes de Ligação de ATP/antagonistas & inibidores
Antineoplásicos/farmacologia
Medições Luminescentes/métodos
Proteínas de Neoplasias/antagonistas & inibidores
[Mh] Termos MeSH secundário: Membro 2 da Subfamília G de Transportadores de Cassetes de Ligação de ATP
Transportadores de Cassetes de Ligação de ATP/genética
Transportadores de Cassetes de Ligação de ATP/metabolismo
Animais
Antineoplásicos/administração & dosagem
Antineoplásicos/isolamento & purificação
Carcinoma Pulmonar de Células não Pequenas/genética
Carcinoma Pulmonar de Células não Pequenas/metabolismo
Carcinoma Pulmonar de Células não Pequenas/patologia
Linhagem Celular
Linhagem Celular Tumoral
Sobrevivência Celular/efeitos dos fármacos
Transplante de Células
Ensaios de Seleção de Medicamentos Antitumorais
Feminino
Glafenina/farmacologia
Seres Humanos
Injeções Intravenosas
Luciferases/genética
Luciferases/metabolismo
Neoplasias Pulmonares/genética
Neoplasias Pulmonares/metabolismo
Neoplasias Pulmonares/patologia
Camundongos
Camundongos Nus
Mitoxantrona/farmacologia
Proteínas de Neoplasias/genética
Proteínas de Neoplasias/metabolismo
Transfecção
Transplante Heterólogo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (ABCG2 protein, human); 0 (ATP Binding Cassette Transporter, Sub-Family G, Member 2); 0 (Antineoplastic Agents); 0 (Neoplasm Proteins); 46HL4I09AH (Glafenine); BZ114NVM5P (Mitoxantrone); EC 1.13.12.- (Luciferases)
[Em] Mês de entrada:0909
[Cu] Atualização por classe:170220
[Lr] Data última revisão:
170220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:090702
[St] Status:MEDLINE
[do] DOI:10.1158/0008-5472.CAN-08-4866


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Fotocópia
[PMID]:14642530
[Au] Autor:Schöber W; Tran QB; Muringaseril M; Wiskirchen J; Kehlbach R; Rodegerdts E; Wiesinger B; Claussen CD; Duda SH
[Ad] Endereço:Eberhard-Karls-Universität, Department of Diagnostic Radiology, Hoppe-Seyler-Str. 3, Tübingen 72076, Germany. Schoeber.wogi@t-online.de
[Ti] Título:Impact of glafenine hydrochloride on human endothelial cells and human vascular smooth muscle cells: a substance reducing proliferation, migration and extracellular matrix synthesis.
[So] Source:Cell Biol Int;27(12):987-96, 2003.
[Is] ISSN:1065-6995
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:The aim of this study was to examine the effects of glafenine hydrochloride (a nonsteroidal anti-inflammatory drug) on proliferation, clonogenic activity, cell-cycle, migration, and the extracellular matrix protein tenascin of human aortic smooth muscle cells (haSMCs) and human endothelial cells (ECs) in vitro.HaSMCs and ECs were seeded in tissue culture flasks. The cells were treated for 4 days with glafenine hydrochloride (10 microM, 50 microM, 100 microM). Half of the treated groups were incubated again with glafenine hydrochloride, the other half received medium free of glafenine hydrochloride every 4 days until day 20. The growth kinetics and clonogenic activity were assessed. Cell cycle distribution was investigated by FACS, migratory ability was evaluated, and effects on extracellular matrix synthesis were assessed by immunofluorescence. Glafenine hydrochloride inhibited the proliferation and clonogenic activity of haSMCs and ECs in a dose-dependent manner. A block in the G2/M phase and a reduction in the G1 phase occurred. The migratory ability of haSMCs was impaired in a dose-dependent manner and the extracellular matrix protein tenascin was reduced. As glafenine hydrochloride has the ability to fully inhibit proliferation and to partially inhibit migration in haSMCs, it could be an interesting substance for further research in the field of restenosis therapy.
[Mh] Termos MeSH primário: Células Endoteliais/efeitos dos fármacos
Matriz Extracelular/metabolismo
Glafenina/farmacologia
Músculo Liso Vascular/efeitos dos fármacos
[Mh] Termos MeSH secundário: Actinas/química
Analgésicos não Entorpecentes/farmacologia
Ciclo Celular
Divisão Celular
Movimento Celular
Separação Celular
Células Cultivadas
Relação Dose-Resposta a Droga
Citometria de Fluxo
Seres Humanos
Cinética
L-Lactato Desidrogenase/metabolismo
Microscopia de Fluorescência
Músculo Liso Vascular/citologia
Miócitos de Músculo Liso/citologia
Fatores de Tempo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Actins); 0 (Analgesics, Non-Narcotic); 46HL4I09AH (Glafenine); EC 1.1.1.27 (L-Lactate Dehydrogenase)
[Em] Mês de entrada:0407
[Cu] Atualização por classe:131121
[Lr] Data última revisão:
131121
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:031204
[St] Status:MEDLINE


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[PMID]:12767387
[Au] Autor:El-Ragehy NA; Ellaithy MM; El-Ghobashy MA
[Ad] Endereço:Analytical Chemistry Department, Faculty of Pharmacy, Cairo University, Kasr El-Aini St., 11562 Cairo, Egypt. n.a.ragehy@mailcity.com
[Ti] Título:Determination of thiocolchicoside in its binary mixtures (thiocolchicoside-glafenine and thiocolchicoside-floctafenine) by TLC-densitometry.
[So] Source:Farmaco;58(6):463-8, 2003 Jun.
[Is] ISSN:0014-827X
[Cp] País de publicação:France
[La] Idioma:eng
[Ab] Resumo:The proposed method is based on TLC separation of thiocolchicoside from its binary mixtures (thiocolchicoside-glafenine and thiocolchicoside-floctafenine) followed by densitometric measurement at 375 nm. Separation was carried out on silica gel plates GF(254) using ethyl acetate:methanol:acetic acid (84:13:3%, v/v/v). Various conditions affecting separation and measurement were studied and optimized. Calibration was performed using third-order polynomial equation. It was found superior to first-order with respect to quantification range (0.25-25 microg per spot), correlation coefficient and standard error of estimation. The proposed method was successfully applied for the determination of thiocolchicoside in its synthetic binary mixtures and commercial tablets. Results were compared with those obtained by reference methods and non-significant difference was obtained regarding accuracy and precision. Assay precision using two-way ANOVA was performed on results of inter- and intra-day applications of the method.
[Mh] Termos MeSH primário: Colchicina/análogos & derivados
Colchicina/análise
Glafenina/análise
ortoaminobenzoatos/análise
[Mh] Termos MeSH secundário: Cromatografia em Camada Delgada/métodos
Colchicina/química
Densitometria/métodos
Glafenina/química
ortoaminobenzoatos/química
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (ortho-Aminobenzoates); 46HL4I09AH (Glafenine); O04HVX6A9Q (floctafenine); SML2Y3J35T (Colchicine); T1X8S697GT (thiocolchicoside)
[Em] Mês de entrada:0402
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:030528
[St] Status:MEDLINE



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