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[PMID]:27774687
[Au] Autor:Clark KM; Jenkins JL; Fedoriw N; Dumont ME
[Ad] Endereço:Department of Pediatrics, University of Rochester Medical Center, Rochester, New York, 14642.
[Ti] Título:Human CaaX protease ZMPSTE24 expressed in yeast: Structure and inhibition by HIV protease inhibitors.
[So] Source:Protein Sci;26(2):242-257, 2017 Feb.
[Is] ISSN:1469-896X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The function and localization of proteins and peptides containing C-terminal "CaaX" (Cys-aliphatic-aliphatic-anything) sequence motifs are modulated by post-translational attachment of isoprenyl groups to the cysteine sulfhydryl, followed by proteolytic cleavage of the aaX amino acids. The zinc metalloprotease ZMPSTE24 is one of two enzymes known to catalyze this cleavage. The only identified target of mammalian ZMPSTE24 is prelamin A, the precursor to the nuclear scaffold protein lamin A. ZMPSTE24 also cleaves prelamin A at a second site 15 residues upstream from the CaaX site. Mutations in ZMPSTE24 result in premature-aging diseases and inhibition of ZMPSTE24 activity has been reported to be an off-target effect of HIV protease inhibitors. We report here the expression (in yeast), purification, and crystallization of human ZMPSTE24 allowing determination of the structure to 2.0 Å resolution. Compared to previous lower resolution structures, the enhanced resolution provides: (1) a detailed view of the active site of ZMPSTE24, including water coordinating the catalytic zinc; (2) enhanced visualization of fenestrations providing access from the exterior to the interior cavity of the protein; (3) a view of the C-terminus extending away from the main body of the protein; (4) localization of ordered lipid and detergent molecules at internal and external surfaces and also projecting through fenestrations; (5) identification of water molecules associated with the surface of the internal cavity. We also used a fluorogenic assay of the activity of purified ZMPSTE24 to demonstrate that HIV protease inhibitors directly inhibit the human enzyme in a manner indicative of a competitive mechanism.
[Mh] Termos MeSH primário: Inibidores da Protease de HIV/química
Proteínas de Membrana/antagonistas & inibidores
Proteínas de Membrana/química
Metaloendopeptidases/antagonistas & inibidores
Metaloendopeptidases/química
[Mh] Termos MeSH secundário: Domínio Catalítico
Seres Humanos
Proteínas de Membrana/genética
Proteínas de Membrana/metabolismo
Metaloendopeptidases/genética
Metaloendopeptidases/metabolismo
Proteínas Recombinantes/química
Proteínas Recombinantes/genética
Proteínas Recombinantes/metabolismo
Saccharomyces cerevisiae/genética
Saccharomyces cerevisiae/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (HIV Protease Inhibitors); 0 (Membrane Proteins); 0 (Recombinant Proteins); EC 3.4.24.- (Metalloendopeptidases); EC 3.4.24.84 (ZMPSTE24 protein, human)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:180201
[Lr] Data última revisão:
180201
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161025
[St] Status:MEDLINE
[do] DOI:10.1002/pro.3074


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[PMID]:29088262
[Au] Autor:Laurence J; Elhadad S; Robison T; Terry H; Varshney R; Woolington S; Ghafoory S; Choi ME; Ahamed J
[Ad] Endereço:Division of Hematology and Medical Oncology, Weill Cornell Medical College (WCMC), New York, New York, United States of America.
[Ti] Título:HIV protease inhibitor-induced cardiac dysfunction and fibrosis is mediated by platelet-derived TGF-ß1 and can be suppressed by exogenous carbon monoxide.
[So] Source:PLoS One;12(10):e0187185, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Human immunodeficiency virus (HIV) infection is an independent risk factor for cardiovascular disease. This risk is magnified by certain antiretrovirals, particularly the protease inhibitor ritonavir, but the pathophysiology of this connection is unknown. We postulated that a major mechanism for antiretroviral-associated cardiac disease is pathologic fibrosis linked to platelet activation with release and activation of transforming growth factor (TGF)-ß1, and that these changes could be modeled in a murine system. We also sought to intervene utilizing inhaled carbon monoxide (CO) as proof-of-concept for therapeutics capable of regulating TGF-ß1 signaling and collagen autophagy. We demonstrate decreased cardiac function indices, including cardiac output, ejection fraction and stroke volume, and prominent cardiac fibrosis, in mice exposed to pharmacological doses of ritonavir. Cardiac output and fibrosis correlated with plasma TGF-ß1 levels. Mice with targeted deletion of TGF-ß1 in megakaryocytes/platelets (PF4CreTgfb1flox/flox) were partially protected from ritonavir-induced cardiac dysfunction and fibrosis. Inhalation of low dose CO (250ppm), used as a surrogate for upregulation of inducible heme oxygenase/endogenous CO pathways, suppressed ritonavir-induced cardiac fibrosis. This occurred in association with modulation of canonical (Smad2) and non-canonical (p38) TGF-ß1 signaling pathways. In addition, CO treatment suppressed the M1 pro-inflammatory subset of macrophages and increased M2c regulatory cells in the hearts of RTV-exposed animals. The effects of CO were dependent upon autophagy as CO did not mitigate ritonavir-induced fibrosis in autophagy-deficient LC3-/- mice. These results suggest that platelet-derived TGF-ß1 contributes to ritonavir-associated cardiac dysfunction and fibrosis, extending the relevance of our findings to other antiretrovirals that also activate platelets. The anti-fibrotic effects of CO are linked to alterations in TGF-ß1 signaling and autophagy, suggesting a proof-of-concept for novel interventions in HIV/antiretroviral therapy-mediated cardiovascular disease.
[Mh] Termos MeSH primário: Plaquetas/metabolismo
Monóxido de Carbono/farmacologia
Inibidores da Protease de HIV/efeitos adversos
Cardiopatias/induzido quimicamente
Miocárdio/patologia
Ritonavir/efeitos adversos
Fator de Crescimento Transformador beta1/metabolismo
[Mh] Termos MeSH secundário: Animais
Plaquetas/efeitos dos fármacos
Débito Cardíaco/efeitos dos fármacos
Ecocardiografia
Fibrose
Cardiopatias/prevenção & controle
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Knockout
Volume Sistólico/efeitos dos fármacos
Fator de Crescimento Transformador beta1/sangue
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (HIV Protease Inhibitors); 0 (Transforming Growth Factor beta1); 7U1EE4V452 (Carbon Monoxide); O3J8G9O825 (Ritonavir)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171113
[Lr] Data última revisão:
171113
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171101
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0187185


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[PMID]:29023508
[Au] Autor:Beckman JA; Wood BR; Ard KL; Price CN; Solomon DA; Zuflacht JP; Milian J; Prenner JC; Sax PE
[Ad] Endereço:Cardiovascular Division, Vanderbilt University Medical Center, Nashville, Tennessee, United States of America.
[Ti] Título:Conflicting effects of atazanavir therapy on atherosclerotic risk factors in stable HIV patients: A randomized trial of regimen switch to atazanavir.
[So] Source:PLoS One;12(10):e0181993, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Bilirubin acts as a potent endogenous antioxidant, with higher concentrations associated with lower rates of CVD; the antiretroviral drug atazanavir (ATV) increases bilirubin levels but may also increase von Willebrand factor levels. We tested the hypothesis that increasing endogenous bilirubin using ATV would improve cardiometabolic risk factors and vascular function in older patients with HIV. Ninety participants were enrolled in two study protocols. In protocol 1, we evaluated markers of inflammation, thrombosis, and conduit artery endothelial function in subjects on non-ATV containing regimens. Participants were randomly assigned to continue baseline treatment or switch to an ATV-based regimen. Measurements were made at baseline and 28 days. In the protocol 2, we enrolled 30 subjects who received atazanavir for more than one year and were compared to the aim 1 protocol subjects at baseline. 60 subjects were enrolled in the first protocol (mean age 53, +/- 6 years), with 31 randomized to ATV and 29 continuing baseline treatment. Atazanavir significantly increased serum total bilirubin levels (p<0.001) and acutely but not chronically plasma total antioxidant capacity (p<0.001). An increase in von Willebrand Factor (p<0.001) and reduction in hs-CRP (p = 0.034) were noted. No changes were seen in either flow-mediated endothelium-dependent or vasodilation. In cross-sectional analysis (second protocol), similar findings were seen in the baseline attributes of non-atazanavir-based and long-term atazanavir users. Increasing serum bilirubin levels with atazanavir in subjects with HIV reduces hs-CRP, temporarily reduces oxidative stress, but increases von Willebrand Factor. Atazanavir does not improve endothelial function of conduit arteries. TRIAL REGISTRATION: ClinicalTrials.gov NCT03019783.
[Mh] Termos MeSH primário: Sulfato de Atazanavir/farmacologia
Aterosclerose/prevenção & controle
Infecções por HIV/tratamento farmacológico
Inibidores da Protease de HIV/farmacologia
HIV-1/efeitos dos fármacos
[Mh] Termos MeSH secundário: Fármacos Anti-HIV/farmacologia
Aterosclerose/etiologia
Bilirrubina/metabolismo
Biomarcadores
Estudos Transversais
Endotélio Vascular/efeitos dos fármacos
Endotélio Vascular/metabolismo
Endotélio Vascular/patologia
Feminino
Infecções por HIV/complicações
Infecções por HIV/virologia
Seres Humanos
Masculino
Meia-Idade
Estresse Oxidativo/efeitos dos fármacos
Fatores de Risco
Carga Viral/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE; RANDOMIZED CONTROLLED TRIAL
[Nm] Nome de substância:
0 (Anti-HIV Agents); 0 (Biomarkers); 0 (HIV Protease Inhibitors); 4MT4VIE29P (Atazanavir Sulfate); RFM9X3LJ49 (Bilirubin)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171105
[Lr] Data última revisão:
171105
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171013
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0181993


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[PMID]:28923796
[Au] Autor:Veilleux O; Lee TC; McDonald EG
[Ad] Endereço:Department of Medicine (Veilleux, Lee, McDonald), McGill University; Clinical Practice Assessment Unit (Lee, McDonald), McGill University Health Centre, Montréal, Que.
[Ti] Título:Rebound adrenal insufficiency after withdrawal of ritonavir in a 65-year-old man using inhaled budesonide.
[So] Source:CMAJ;189(37):E1188-E1191, 2017 09 18.
[Is] ISSN:1488-2329
[Cp] País de publicação:Canada
[La] Idioma:eng
[Mh] Termos MeSH primário: Insuficiência Adrenal/etiologia
Asma/tratamento farmacológico
Budesonida/administração & dosagem
Infecções por HIV/tratamento farmacológico
Ritonavir/uso terapêutico
Suspensão de Tratamento
[Mh] Termos MeSH secundário: Administração por Inalação
Idoso
Asma/complicações
Broncodilatadores/administração & dosagem
Infecções por HIV/complicações
Inibidores da Protease de HIV
Seres Humanos
Masculino
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Bronchodilator Agents); 0 (HIV Protease Inhibitors); 51333-22-3 (Budesonide); O3J8G9O825 (Ritonavir)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171102
[Lr] Data última revisão:
171102
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170920
[St] Status:MEDLINE
[do] DOI:10.1503/cmaj.170415


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[PMID]:28739156
[Au] Autor:Funicello M; Chiummiento L; Tramutola F; Armentano MF; Bisaccia F; Miglionico R; Milella L; Benedetti F; Berti F; Lupattelli P
[Ad] Endereço:Dipartimento di Scienze, Università della Basilicata, Via Ateneo Lucano 10, 85100 Potenza, Italy.
[Ti] Título:Synthesis and biological evaluation in vitro and in mammalian cells of new heteroaryl carboxyamides as HIV-protease inhibitors.
[So] Source:Bioorg Med Chem;25(17):4715-4722, 2017 Sep 01.
[Is] ISSN:1464-3391
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:New heteroaryl HIV-protease inhibitors bearing a carboxyamide spacer were synthesized in few steps and high yield, from commercially available homochiral epoxides. Different substitution patterns were introduced onto a given isopropanoyl-sulfonamide core modifying the type of heteroarene and the central core, with the presence of either H or benzyl group. Their in vitro inhibition activity against recombinant protease showed a general beneficial effect of carboxyamide moiety, the IC values ranging between 1 and 15nM. In particular benzofuryl derivatives showed IC values among the best for such structurally simple inhibitors. Docking analysis allowed to identify the favorable situation of such benzofuryl derivatives in terms of number of interactions in the active site, supporting the experimental results on activity. The inhibition activity of such molecules has been also evaluated in HEK293 cells expressing the protease fused to green fluorescent protein, by western blotting analysis, fluorescence microscopy and cytofluorimetry.
[Mh] Termos MeSH primário: Amidas/química
Inibidores da Protease de HIV/síntese química
Protease de HIV/metabolismo
[Mh] Termos MeSH secundário: Amidas/síntese química
Amidas/farmacologia
Sítios de Ligação
Sobrevivência Celular/efeitos dos fármacos
Células HEK293
HIV/efeitos dos fármacos
HIV/enzimologia
Protease de HIV/química
Inibidores da Protease de HIV/farmacologia
Seres Humanos
Concentração Inibidora 50
Microscopia de Fluorescência
Simulação de Acoplamento Molecular
Estrutura Terciária de Proteína
Relação Estrutura-Atividade
Transfecção
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Amides); 0 (HIV Protease Inhibitors); EC 3.4.23.- (HIV Protease)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170926
[Lr] Data última revisão:
170926
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170726
[St] Status:MEDLINE


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[PMID]:28659616
[Au] Autor:Barzi M; Pankowicz FP; Zorman B; Liu X; Legras X; Yang D; Borowiak M; Bissig-Choisat B; Sumazin P; Li F; Bissig KD
[Ad] Endereço:Center for Cell and Gene Therapy, Stem Cells and Regenerative Medicine Center, Baylor College of Medicine, Houston, TX-77030, USA.
[Ti] Título:A novel humanized mouse lacking murine P450 oxidoreductase for studying human drug metabolism.
[So] Source:Nat Commun;8(1):39, 2017 06 28.
[Is] ISSN:2041-1723
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Only one out of 10 drugs in development passes clinical trials. Many fail because experimental animal models poorly predict human xenobiotic metabolism. Human liver chimeric mice are a step forward in this regard, as the human hepatocytes in chimeric livers generate human metabolites, but the remaining murine hepatocytes contain an expanded set of P450 cytochromes that form the major class of drug-metabolizing enzymes. We therefore generated a conditional knock-out of the NADPH-P450 oxidoreductase (Por) gene combined with Il2rg /Rag2 /Fah (PIRF) mice. Here we show that homozygous PIRF mouse livers are readily repopulated with human hepatocytes, and when the murine Por gene is deleted (<5%), they predominantly use human cytochrome metabolism. When given the anticancer drug gefitinib or the retroviral drug atazanavir, the Por-deleted humanized PIRF mice develop higher levels of the major human metabolites than current models. Humanized, murine Por-deficient PIRF mice can thus predict human drug metabolism and should be useful for preclinical drug development.Human liver chimeric mice are increasingly used for drug testing in preclinical development, but express residual murine p450 cytochromes. Here the authors generate mice lacking the Por gene in the liver, and show that human cytochrome metabolism is used following repopulation with human hepatocytes.
[Mh] Termos MeSH primário: Sulfato de Atazanavir/metabolismo
Sistema Enzimático do Citocromo P-450/metabolismo
Quinazolinas/metabolismo
[Mh] Termos MeSH secundário: Animais
Antineoplásicos/metabolismo
Quimera
Sistema Enzimático do Citocromo P-450/genética
Citocromos/metabolismo
Feminino
Genótipo
Inibidores da Protease de HIV/metabolismo
Seres Humanos
Fígado/enzimologia
Fígado/metabolismo
Masculino
Camundongos
Camundongos Endogâmicos
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Antineoplastic Agents); 0 (Cytochromes); 0 (HIV Protease Inhibitors); 0 (Quinazolines); 4MT4VIE29P (Atazanavir Sulfate); 9035-51-2 (Cytochrome P-450 Enzyme System); S65743JHBS (gefitinib)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171107
[Lr] Data última revisão:
171107
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170630
[St] Status:MEDLINE
[do] DOI:10.1038/s41467-017-00049-x


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[PMID]:28647214
[Au] Autor:Ahammed V; Narayan R; Paul J; Nayak Y; Roy B; Shavi GV; Nayak UY
[Ad] Endereço:Department of Pharmaceutics, Manipal University, Manipal 576104, India.
[Ti] Título:Development and in vivo evaluation of functionalized ritonavir proliposomes for lymphatic targeting.
[So] Source:Life Sci;183:11-20, 2017 Aug 15.
[Is] ISSN:1879-0631
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:AIMS: The aim of the present work was to prepare, characterize, and evaluate proliposomes containing lipophilic prodrug ritonavir for targeting towards CD4+ T cells in the lymphatic system. MATERIALS AND METHODS: The liposomes were prepared by lipid thin film hydration method and lyophilized in the presence of cryoprotectant mannitol to obtain proliposomes. The optimized proliposomes by Central Composite Design, were surface modified with biotin. The proliposomes were evaluated for particle size, zeta potential, polydispersity index (PDI), entrapment efficiency, in vitro drug release, in vivo pharmacokinetics and biodistribution studies. KEY FINDINGS: The mean particle size was found to be in the range of 126.6 to 306.2nm with PDI of 0.340-1.00. The entrapment efficiency was found to be in the range of 18.9 to 86.2%. The formulations showed a zeta potential in the range of -18.1 to -20.2mv. Biotinylated proliposomes (LIP-5B) were in the size of 149.8±6.8nm with entrapment efficiency 61.6%. The % CDR of pure drug, conventional, biotinylated proliposome in 3h was found to be 58.3, 82.04, and 95.9% respectively. In vitro drug release and in vivo pharmacokinetics of the pure drug, optimized conventional proliposomes (LIP-5) and biotin proliposomes (LIP-5B) were executed. SIGNIFICANCE: The AUC for the liposomes were found to be much higher in the spleen and thymus compared to that in the plasma which indicated that the developed formulations enhance the bioavailability and target specificity compared to that of the pure drug thereby enhancing bioavailability at target site.
[Mh] Termos MeSH primário: Biotina/química
Linfócitos T CD4-Positivos/metabolismo
Sistemas de Liberação de Medicamentos
Inibidores da Protease de HIV/administração & dosagem
Ritonavir/administração & dosagem
[Mh] Termos MeSH secundário: Animais
Disponibilidade Biológica
Química Farmacêutica/métodos
Liberação Controlada de Fármacos
Inibidores da Protease de HIV/farmacocinética
Lipídeos
Lipossomos
Tamanho da Partícula
Pró-Fármacos
Ratos
Ratos Wistar
Ritonavir/farmacocinética
Baço/metabolismo
Timo/metabolismo
Distribuição Tecidual
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (HIV Protease Inhibitors); 0 (Lipids); 0 (Liposomes); 0 (Prodrugs); 6SO6U10H04 (Biotin); O3J8G9O825 (Ritonavir)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170808
[Lr] Data última revisão:
170808
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170626
[St] Status:MEDLINE


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[PMID]:28622345
[Au] Autor:Zeng P; Liu Y; He M; Wang J; Keating S; Mao W; Huang M; Ma H; He W; Bi X; Liao D; Busch M; Ness P; Liu J; Shan H; NHLBI Recipient Epidemiology and Donor Evaluation Study-III program
[Ad] Endereço:West China School of Public Health, Sichuan University, Chengdu, Sichuan, China.
[Ti] Título:The infection staging and profile of genotypic distribution and drug resistance mutation among the human immunodeficiency virus-1 infected blood donors from five Chinese blood centers, 2012-2014.
[So] Source:PLoS One;12(6):e0179328, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The increasing complexity and diversity of the human immunodeficiency virus-1 (HIV-1) infections challenge the disease control and anti-retrovirus treatment in China. The infection stages and molecular characteristics of HIV-1 from infected Chinese blood donors were examined to shed light on the HIV genotype distribution and the status of drug resistance mutations (DRMs) in the changing HIV epidemic in China. Western blot (WB) confirmed HIV-1 positive plasma samples were collected from blood donors at five Chinese blood centers from April 16, 2012, through June 30, 2014. The HIV infection stages were determined using the Lag-avidity assay. HIV Pol regions including whole protease and partial reverse transcriptase (RT) were amplified and sequenced to establish the profile of genotype distribution and drug resistance mutations (DRMs). Viral loads were determined using the ROCHE COBAS system. Of the 259 HIV-1 positive samples tested by the Lag-avidity assay, 23.6% (61/259) were identified as recent infections. A total of 205 amplified sequences displayed the following genotype distributions: circulating recombinant form (CRF) 07_BC (61.5%), CRF08_BC (8.3%), CRF01_AE (20%), B (6.3%), and 01B (3.9%). There was no significant difference in genotype distribution between recent and long-term infections. 31 DRMs were identified from 27 samples including four protease inhibitors (PIs) accessory DRMs, two PIs major DRMs (M46I), two nucleoside RT inhibitors DRMs (K219R and K70Q), and 23 nonnucleoside RT inhibitors DRMs. 27 samples had DRMs, yielding a drug resistance prevalence of 13.2% (27/205). Our findings provide important information for developing strategies for comprehensive HIV control and improving anti-retroviral treatment in China.
[Mh] Termos MeSH primário: Bancos de Sangue
Doadores de Sangue
Farmacorresistência Viral/genética
Genótipo
Infecções por HIV/genética
Protease de HIV/genética
Transcriptase Reversa do HIV/genética
HIV-1/genética
Mutação
[Mh] Termos MeSH secundário: Adolescente
Adulto
Grupo com Ancestrais do Continente Asiático
China/epidemiologia
Feminino
Infecções por HIV/tratamento farmacológico
Infecções por HIV/epidemiologia
Inibidores da Protease de HIV/administração & dosagem
Seres Humanos
Masculino
Meia-Idade
Inibidores da Transcriptase Reversa/administração & dosagem
Carga Viral/métodos
[Pt] Tipo de publicação:CLINICAL TRIAL; JOURNAL ARTICLE; MULTICENTER STUDY
[Nm] Nome de substância:
0 (HIV Protease Inhibitors); 0 (Reverse Transcriptase Inhibitors); EC 2.7.7.- (reverse transcriptase, Human immunodeficiency virus 1); EC 2.7.7.49 (HIV Reverse Transcriptase); EC 3.4.23.- (HIV Protease)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170914
[Lr] Data última revisão:
170914
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170617
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0179328


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[PMID]:28579422
[Au] Autor:Santoriello D; Al-Nabulsi M; Reddy A; Salamera J; D'Agati VD; Markowitz GS
[Ad] Endereço:Department of Pathology & Cell Biology, Columbia University Medical Center, New York, NY. Electronic address: ds3356@cumc.columbia.edu.
[Ti] Título:Atazanavir-Associated Crystalline Nephropathy.
[So] Source:Am J Kidney Dis;70(4):576-580, 2017 Oct.
[Is] ISSN:1523-6838
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Crystalline nephropathy can occur following treatment with multiple therapeutic agents. We describe a human immunodeficiency virus (HIV)-infected patient treated for 2 years with combination antiretroviral therapy including atazanavir (ATV). Kidney biopsy revealed a crystalline nephropathy associated with diffuse chronic and granulomatous interstitial inflammation. Following the biopsy, treatment with ATV was discontinued and kidney function returned to pretreatment baseline levels. ATV, which has a well-established association with nephrolithiasis, is a rare but important cause of crystalline nephropathy. Recognition of this association and prompt withdrawal of the offending agent are critical to optimize outcomes.
[Mh] Termos MeSH primário: Sulfato de Atazanavir/efeitos adversos
Inibidores da Protease de HIV/efeitos adversos
Nefropatias/induzido quimicamente
[Mh] Termos MeSH secundário: Cristalização
Seres Humanos
Masculino
Meia-Idade
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (HIV Protease Inhibitors); 4MT4VIE29P (Atazanavir Sulfate)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171012
[Lr] Data última revisão:
171012
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170606
[St] Status:MEDLINE


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[PMID]:28554091
[Au] Autor:Bai X; Yang Z; Zhu M; Dong B; Zhou L; Zhang G; Wang J; Wang Y
[Ad] Endereço:Institute of Medicinal Biotechnology, Chinese Academy of Medical Science and Peking Union Medical College, Beijing 100050, China.
[Ti] Título:Design and synthesis of potent HIV-1 protease inhibitors with (S)-tetrahydrofuran-tertiary amine-acetamide as P2-ligand: Structure-activity studies and biological evaluation.
[So] Source:Eur J Med Chem;137:30-44, 2017 Sep 08.
[Is] ISSN:1768-3254
[Cp] País de publicação:France
[La] Idioma:eng
[Ab] Resumo:The design, synthesis, and SAR study of a new series of HIV-1 protease inhibitors incorporating stereochemically defined tetrahydrofuran-tertiary amine-acetamide P2-ligand are described. Various substituent effects on the tertiary amine P2-ligand and phenylsulfonamide P2'-ligand were investigated to maximize the ligand-binding site interactions in the protease active site. Most of inhibitors displayed low nanomolar to subnanomolar inhibitory potency. Inhibitor 20e containing N-(S-tetrahydrofuran)-N-(2-methoxyethyl)acetamide as P2-ligand along with 4-methoxylphenylsulfonamide as P2'-ligand displayed the most potent enzyme inhibitory activity (IC = 0.35 nM) and remarkably low cytotoxicity (CC = 305 µM).
[Mh] Termos MeSH primário: Acetamidas/farmacologia
Aminas/farmacologia
Desenho de Drogas
Furanos/farmacologia
Inibidores da Protease de HIV/farmacologia
Protease de HIV/metabolismo
[Mh] Termos MeSH secundário: Acetamidas/química
Aminas/química
Animais
Linhagem Celular
Sobrevivência Celular/efeitos dos fármacos
Relação Dose-Resposta a Droga
Furanos/química
Inibidores da Protease de HIV/síntese química
Inibidores da Protease de HIV/química
Seres Humanos
Ligantes
Camundongos
Estrutura Molecular
Coelhos
Estereoisomerismo
Relação Estrutura-Atividade
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Acetamides); 0 (Amines); 0 (Furans); 0 (HIV Protease Inhibitors); 0 (Ligands); 3N8FZZ6PY4 (tetrahydrofuran); 8XOE1JSO29 (acetamide); EC 3.4.23.- (HIV Protease); EC 3.4.23.- (p16 protease, Human immunodeficiency virus 1)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170920
[Lr] Data última revisão:
170920
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170530
[St] Status:MEDLINE



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