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[PMID]:29324623
[Au] Autor:Hussar DA
[Ad] Endereço:Remington Professor of Pharmacy Philadelphia College of Pharmacy University of the Sciences Philadelphia, Pa.
[Ti] Título:New Drugs 2018, part 1.
[So] Source:Nursing;48(2):36-44, 2018 Feb.
[Is] ISSN:1538-8689
[Cp] País de publicação:United States
[La] Idioma:eng
[Mh] Termos MeSH primário: Aprovação de Drogas
[Mh] Termos MeSH secundário: Anticorpos Monoclonais/uso terapêutico
Anticorpos Neutralizantes/uso terapêutico
Antipirina/análogos & derivados
Antipirina/uso terapêutico
Benzamidas/uso terapêutico
Benzimidazóis/uso terapêutico
Carbamatos/uso terapêutico
Combinação de Medicamentos
Compostos Heterocíclicos de 4 ou mais Anéis/uso terapêutico
Seres Humanos
Compostos Macrocíclicos/uso terapêutico
Naltrexona/análogos & derivados
Naltrexona/uso terapêutico
Peptídeos Natriuréticos/uso terapêutico
Piridinas/uso terapêutico
Quinoxalinas/uso terapêutico
Sofosbuvir/uso terapêutico
Sulfonamidas/uso terapêutico
Estados Unidos
United States Food and Drug Administration
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (ABT-493); 0 (Antibodies, Monoclonal); 0 (Antibodies, Neutralizing); 0 (Benzamides); 0 (Benzimidazoles); 0 (Carbamates); 0 (Drug Combinations); 0 (Heterocyclic Compounds, 4 or More Rings); 0 (Macrocyclic Compounds); 0 (Natriuretic Peptides); 0 (Pyridines); 0 (Quinoxalines); 0 (Sulfonamides); 0 (bezlotoxumab); 0 (naldemedine); 0 (pibrentasvir); 0 (voxilaprevir); 5S6W795CQM (Naltrexone); 74RWP7W0J9 (betrixaban); 7IK8Z952OK (plecanatide); KCU0C7RS7Z (velpatasvir); S798V6YJRP (phenylmethylpyrazolone); T3CHA1B51H (Antipyrine); WJ6CA3ZU8B (Sofosbuvir)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180223
[Lr] Data última revisão:
180223
[Sb] Subgrupo de revista:N
[Da] Data de entrada para processamento:180112
[St] Status:MEDLINE
[do] DOI:10.1097/01.NURSE.0000529803.83288.e1


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[PMID]:28973341
[Au] Autor:Akiyama G; Azuchi Y; Guo X; Noro T; Kimura A; Harada C; Namekata K; Harada T
[Ad] Endereço:Visual Research Project, Tokyo Metropolitan Institute of Medical Science, Tokyo, Japan.
[Ti] Título:Edaravone Prevents Retinal Degeneration in Adult Mice Following Optic Nerve Injury.
[So] Source:Invest Ophthalmol Vis Sci;58(11):4908-4914, 2017 Sep 01.
[Is] ISSN:1552-5783
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Purpose: To assess the therapeutic potential of edaravone, a free radical scavenger that is used for the treatment of acute brain infarction and amyotrophic lateral sclerosis, in a mouse model of optic nerve injury (ONI). Methods: Two microliters of edaravone (7.2 mM) or vehicle were injected intraocularly 3 minutes after ONI. Optical coherence tomography, retrograde labeling of retinal ganglion cells (RGCs), histopathology, and immunohistochemical analyses of phosphorylated apoptosis signal-regulating kinase-1 (ASK1) and p38 mitogen-activated protein kinase (MAPK) in the retina were performed after ONI. Reactive oxygen species (ROS) levels were assessed with a CellROX Green Reagent. Results: Edaravone ameliorated ONI-induced ROS production, RGC death, and inner retinal degeneration. Also, activation of the ASK1-p38 MAPK pathway that induces RGC death following ONI was suppressed with edaravone treatment. Conclusions: The results of this study suggest that intraocular administration of edaravone may be a useful treatment for posttraumatic complications.
[Mh] Termos MeSH primário: Antipirina/análogos & derivados
Depuradores de Radicais Livres/farmacologia
Traumatismos do Nervo Óptico/tratamento farmacológico
Degeneração Retiniana/prevenção & controle
[Mh] Termos MeSH secundário: Animais
Antipirina/farmacologia
Modelos Animais de Doenças
Imuno-Histoquímica
Injeções Intraoculares
MAP Quinase Quinase 1/metabolismo
MAP Quinase Quinase Quinase 5/metabolismo
Camundongos
Camundongos Endogâmicos C57BL
Traumatismos do Nervo Óptico/metabolismo
Traumatismos do Nervo Óptico/patologia
Espécies Reativas de Oxigênio/metabolismo
Retina/metabolismo
Degeneração Retiniana/patologia
Células Ganglionares da Retina/patologia
Tomografia de Coerência Óptica
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Free Radical Scavengers); 0 (Reactive Oxygen Species); EC 2.7.11.25 (MAP Kinase Kinase Kinase 5); EC 2.7.12.2 (MAP Kinase Kinase 1); S798V6YJRP (phenylmethylpyrazolone); T3CHA1B51H (Antipyrine)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171006
[Lr] Data última revisão:
171006
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171004
[St] Status:MEDLINE
[do] DOI:10.1167/iovs.17-22250


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[PMID]:28942283
[Au] Autor:Lin H; Ma X; Wang BC; Zhao L; Liu JX; Pu FF; Hu YQ; Hu HZ; Shao ZW
[Ad] Endereço:Department of Orthopedic Surgery, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, China.
[Ti] Título:Edaravone ameliorates compression-induced damage in rat nucleus pulposus cells.
[So] Source:Life Sci;189:76-83, 2017 Nov 15.
[Is] ISSN:1879-0631
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:AIMS: Edaravone is a strong free radical scavenger most used for treating acute ischemic stroke. In this study we investigated the protective effects and underlying mechanisms of edaravone on compression-induced damage in rat nucleus pulposus (NP) cells. MATERIALS AND METHODS: Cell viability was determined using MTT assay methods. NP cell apoptosis was measured by Hoechst 33,258 staining and Annexin V/PI double staining. Intracellular reactive oxygen species (ROS), mitochondrial membrane potential (MMP), and intracellular calcium ([Ca ] ) were determined by fluorescent probes DCFH-DA, JC-1 and Fluo-3/AM, respectively. Apoptosis-related proteins (cleaved caspase-3, cytosolic cytochrome c, Bax and Bcl-2) and extracellular matrix proteins (aggrecan and collagen II) were analyzed by western blot. KEY FINDINGS: Edaravone attenuated the compression-induced decrease in viability of NP cells in a dose-dependent manner. 33,258 and Annexin V/PI double staining showed that edaravone protected NP cells from compression-induced apoptosis. Further studies confirmed that edaravone protected NP cells against compression-induced mitochondrial pathway of apoptosis by inhibiting overproduction of ROS, collapse of MMP and overload of [Ca ] . In addition, edaravone promoted the expression of aggrecan and collagen II in compression-treated NP cells. SIGNIFICANCE: These results strongly indicate that edaravone ameliorates compression-induced damage in rat nucleus pulposus cells. Edaravone could be a potential new drug for treatment of IDD.
[Mh] Termos MeSH primário: Antipirina/análogos & derivados
Apoptose/efeitos dos fármacos
Sobrevivência Celular/efeitos dos fármacos
Depuradores de Radicais Livres/farmacologia
Núcleo Pulposo/efeitos dos fármacos
[Mh] Termos MeSH secundário: Agrecanas/genética
Animais
Antipirina/administração & dosagem
Antipirina/farmacologia
Células Cultivadas
Colágeno Tipo II/genética
Relação Dose-Resposta a Droga
Depuradores de Radicais Livres/administração & dosagem
Regulação da Expressão Gênica/efeitos dos fármacos
Degeneração do Disco Intervertebral/tratamento farmacológico
Degeneração do Disco Intervertebral/fisiopatologia
Potencial da Membrana Mitocondrial
Núcleo Pulposo/patologia
Ratos
Ratos Sprague-Dawley
Espécies Reativas de Oxigênio/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Aggrecans); 0 (Collagen Type II); 0 (Free Radical Scavengers); 0 (Reactive Oxygen Species); S798V6YJRP (phenylmethylpyrazolone); T3CHA1B51H (Antipyrine)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171023
[Lr] Data última revisão:
171023
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170925
[St] Status:MEDLINE


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[PMID]:28522181
[Au] Autor:Writing Group; Edaravone (MCI-186) ALS 19 Study Group
[Ti] Título:Safety and efficacy of edaravone in well defined patients with amyotrophic lateral sclerosis: a randomised, double-blind, placebo-controlled trial.
[So] Source:Lancet Neurol;16(7):505-512, 2017 Jul.
[Is] ISSN:1474-4465
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: In a previous phase 3 study in patients with amyotrophic lateral sclerosis (ALS), edaravone did not show a significant difference in the Revised ALS Functional Rating Scale (ALSFRS-R) score compared with placebo. Post-hoc analysis of these data revealed that patients in an early stage with definite or probable diagnosis of ALS, defined by the revised El Escorial criteria, who met a select set of inclusion criteria showed a greater magnitude of effect than did the full study population. We aimed to substantiate this post-hoc result and assess safety and efficacy of edaravone in a phase 3 trial that focused on patients with early stage ALS who met the post-hoc analysis inclusion criteria. METHODS: In this phase 3, randomised, double-blind, parallel-group study, patients aged 20-75 years with ALS of grade 1 or 2 in the Japan ALS Severity Classification, scores of at least 2 points on all 12 items of ALSFRS-R, forced vital capacity of 80% or more, definite or probable ALS according to the revised El Escorial criteria, and disease duration of 2 years or less were recruited from 31 hospitals in Japan. Eligible patients also had a decrease of 1-4 points in the ALSFRS-R score during a 12-week observation period before randomisation. Patients meeting all criteria were then randomly assigned 1:1 to receive 60 mg intravenous edaravone or intravenous saline placebo for 6 cycles (4 weeks per cycle with 2 weeks on, 2 weeks off) for a total treatment duration of 24 weeks. In cycle 1, the study drug or placebo was administered once per day for 14 days within a 14 day period, followed by the drug-free period. In cycle 2 and thereafter, the study drug or placebo was administered for 10 days within a 14 day period, followed by a 2 week drug-free period. Participants and investigators, including those assessing outcomes, were masked to treatment allocation. The primary efficacy outcome was the change in ALSFRS-R score from the baseline to 24 weeks (or at discontinuation if this was after the third cycle) after randomisation. The primary outcome was assessed in all patients who had received at least one treatment infusion, had at least one assessment post-baseline, and reached the end of cycle 3. For patients with missing values at the end of cycle 6, data were imputed by the last observation carried forward (LOCF) method, provided the patients had completed at least cycle 3. Safety was assessed in all patients who had received at least one treatment infusion and had at least one assessment post-baseline. This trial is registered with ClinicalTrials.gov, NCT01492686. FINDINGS: Between Nov 28, 2011, and Sept 3, 2014, we screened 213 patients, and enrolled 192 as potential participants. Of these, 137 patients completed the observation period: 69 were randomly assigned to receive edaravone, and 68 were randomly assigned to receive placebo. 68 patients taking edaravone and 66 taking placebo were included in the primary efficacy analysis. For the primary outcome, the change in ALSFRS-R score was -5·01 (SE 0·64) in the edavarone group and -7·50 (0·66) in the placebo group. The least-squares mean difference between groups was 2·49 (SE 0·76, 95% CI 0·99-3·98; p=0·0013) in favour of edaravone. Treatment-emergent adverse events were reported in 58 (84%) patients receiving edaravone and 57 (84%) patients receiving placebo. 11 (16%) patients taking edaravone and 16 (24%) taking placebo had serious adverse events, and one (1%) patient receiving edaravone and four (6%) patients receiving placebo had adverse events (one dysphagia in edaravone group and one dyspnoea, two respiratory disorder, and one rash in the placebo group) that led to withdrawal. INTERPRETATION: Edaravone showed efficacy in a small subset of people with ALS who met criteria identified in post-hoc analysis of a previous phase 3 study, showing a significantly smaller decline of ALSFRS-R score compared with placebo. There is no indication that edaravone might be effective in a wider population of patients with ALS who do not meet the criteria. FUNDING: Mitsubishi Tanabe Pharma Corporation.
[Mh] Termos MeSH primário: Esclerose Amiotrófica Lateral/diagnóstico
Esclerose Amiotrófica Lateral/tratamento farmacológico
Antipirina/análogos & derivados
Depuradores de Radicais Livres/farmacologia
Avaliação de Resultados (Cuidados de Saúde)
Índice de Gravidade de Doença
[Mh] Termos MeSH secundário: Adulto
Idoso
Antipirina/administração & dosagem
Antipirina/efeitos adversos
Antipirina/farmacologia
Método Duplo-Cego
Feminino
Depuradores de Radicais Livres/administração & dosagem
Depuradores de Radicais Livres/efeitos adversos
Seres Humanos
Masculino
Meia-Idade
Adulto Jovem
[Pt] Tipo de publicação:CLINICAL TRIAL, PHASE III; JOURNAL ARTICLE; RANDOMIZED CONTROLLED TRIAL
[Nm] Nome de substância:
0 (Free Radical Scavengers); S798V6YJRP (phenylmethylpyrazolone); T3CHA1B51H (Antipyrine)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170719
[Lr] Data última revisão:
170719
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170520
[St] Status:MEDLINE


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[PMID]:28406335
[Au] Autor:Sawada H
[Ad] Endereço:a Department of Neurology , Utano National Hospital , Kyoto , Japan.
[Ti] Título:Clinical efficacy of edaravone for the treatment of amyotrophic lateral sclerosis.
[So] Source:Expert Opin Pharmacother;18(7):735-738, 2017 May.
[Is] ISSN:1744-7666
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:INTRODUCTION: Amyotrophic lateral sclerosis (ALS) is a progressive, fatal, neurodegenerative disease. Although the pathogenesis remains unresolved, oxidative stress is known to play a pivotal role. Edaravone works in the central nervous system as a potent scavenger of oxygen radicals. In ALS mouse models, edaravone suppresses motor functional decline and nitration of tyrosine residues in the cerebrospinal fluid. Areas covered: Three clinical trials, one phase II open-label trial, and two phase III placebo-control randomized trials were reviewed. In all trials, the primary outcome measure was the changes in scores on the revised ALS functional rating scale (ALSFRS-R) to evaluate motor function of patients. Expert opinion: The phase II open label trial suggested that edaravone is safe and effective in ALS, markedly reducing 3-nitrotyrosine levels in the cerebrospinal fluid. One of the two randomized controlled trials showed beneficial effects in ALSFRS-R, although the differences were not significant. The last trial demonstrated that edaravone provided significant efficacy in ALSFRS-R scores over 24 weeks where concomitant use of riluzole was permitted. Eligibility was restricted to patients with a relatively short disease duration and preserved vital capacity. Therefore, combination therapy with edaravone and riluzole should be considered earlier.
[Mh] Termos MeSH primário: Esclerose Amiotrófica Lateral/tratamento farmacológico
Antipirina/análogos & derivados
Depuradores de Radicais Livres/uso terapêutico
[Mh] Termos MeSH secundário: Animais
Antipirina/uso terapêutico
Modelos Animais de Doenças
Seres Humanos
Ensaios Clínicos Controlados Aleatórios como Assunto
Fatores de Tempo
Resultado do Tratamento
Tirosina/análogos & derivados
Tirosina/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Free Radical Scavengers); 3604-79-3 (3-nitrotyrosine); 42HK56048U (Tyrosine); S798V6YJRP (phenylmethylpyrazolone); T3CHA1B51H (Antipyrine)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170724
[Lr] Data última revisão:
170724
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170414
[St] Status:MEDLINE
[do] DOI:10.1080/14656566.2017.1319937


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[PMID]:28382161
[Au] Autor:Jin Q; Cai Y; Li S; Liu H; Zhou X; Lu C; Gao X; Qian J; Zhang J; Ju S; Li C
[Ad] Endereço:Key Laboratory of Smart Drug Delivery, Ministry of Education, School of Pharmacy, Fudan University, 826 Zhangheng Road, Shanghai 201203, P. R. China.
[Ti] Título:Edaravone-Encapsulated Agonistic Micelles Rescue Ischemic Brain Tissue by Tuning Blood-Brain Barrier Permeability.
[So] Source:Theranostics;7(4):884-898, 2017.
[Is] ISSN:1838-7640
[Cp] País de publicação:Australia
[La] Idioma:eng
[Ab] Resumo:Thrombolysis has been a standard treatment for ischemic stroke. However, only 2-7% patients benefit from it because the thrombolytic agent has to be injected within 4.5 h after the onset of symptoms to avoid the increasing risk of intracerebral hemorrhage. As the only clinically approved neuroprotective drug, edaravone (EDV) rescues ischemic brain tissues by eradicating over-produced reactive oxygen species (ROS) without the limitation of therapeutic time-window. However, EDV's short circulation half-life and inadequate cerebral uptake attenuate its therapeutic efficacy. Here we developed an EDV-encapsulated agonistic micelle (EDV-AM) to specifically deliver EDV into brain ischemia by actively tuning blood-brain barrier (BBB) permeability. The EDV-AM actively up-regulated endothelial monolayer permeability . HPLC studies showed that EDV-AM delivered more EDV into brain ischemia than free EDV after intravenous injection. Magnetic resonance imaging also demonstrated that EDV-AM more rapidly salvaged ischemic tissue than free EDV. Diffusion tensor imaging indicated the highest efficiency of EDV-AM in accelerating axonal remodeling in the ipsilesional white matter and improving functional behaviors of ischemic stroke models. The agonistic micelle holds promise to improve the therapeutic efficiency of ischemic stroke patients who miss the thrombolytic treatment.
[Mh] Termos MeSH primário: Antipirina/análogos & derivados
Barreira Hematoencefálica/efeitos dos fármacos
Isquemia Encefálica/tratamento farmacológico
Depuradores de Radicais Livres/administração & dosagem
Micelas
Fármacos Neuroprotetores/administração & dosagem
Permeabilidade/efeitos da radiação
[Mh] Termos MeSH secundário: Animais
Antipirina/administração & dosagem
Antipirina/farmacocinética
Isquemia Encefálica/diagnóstico por imagem
Células Cultivadas
Células Endoteliais/efeitos dos fármacos
Depuradores de Radicais Livres/farmacocinética
Imagem por Ressonância Magnética
Camundongos Endogâmicos ICR
Fármacos Neuroprotetores/farmacocinética
Resultado do Tratamento
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Free Radical Scavengers); 0 (Micelles); 0 (Neuroprotective Agents); S798V6YJRP (phenylmethylpyrazolone); T3CHA1B51H (Antipyrine)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171024
[Lr] Data última revisão:
171024
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170407
[St] Status:MEDLINE
[do] DOI:10.7150/thno.18219


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[PMID]:28346481
[Au] Autor:Li Y; Liu H; Zeng W; Wei J
[Ad] Endereço:Department of Ophthalmology, The First Affiliated Hospital and College of Clinical Medicine of Henan University of Science and Technology, Luoyang, China.
[Ti] Título:Edaravone protects against hyperosmolarity-induced oxidative stress and apoptosis in primary human corneal epithelial cells.
[So] Source:PLoS One;12(3):e0174437, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:An increase in the osmolarity of tears induced by excessive evaporation of the aqueous tear phase is a major pathological mechanism behind dry eye. Exposure of epithelial cells on the surface of the human eye to hyperosmolarity leads to oxidative stress, mitochondrial dysfunction, and apoptosis. Edaravone, a hydroxyl radical scavenging agent, is clinically used to reduce neuronal damage following ischemic stroke. In this study, we found that treatment with hyperosmotic media at 400 and 450 mOsM increased the levels of ROS and mitochondrial oxidative damage, which were ameliorated by edaravone treatment in a dose-dependent manner. We also found that edaravone could improve mitochondrial function in HCEpiCs by increasing the levels of ATP and mitochondrial membrane potential. MTT and LDH assays indicated that edaravone could attenuate hyperosmolarity-induced cell death. It was found that edaravone prevented apoptosis by decreasing the level of cleaved caspase-3, and attenuating the release of cytochrome C. Mechanistically, we found that edaravone augmented the expression of Nrf2 and its target genes, such as HO-1, GPx-1, and GCLC.
[Mh] Termos MeSH primário: Antipirina/análogos & derivados
Apoptose/efeitos dos fármacos
Células Epiteliais/efeitos dos fármacos
Epitélio Anterior/efeitos dos fármacos
Depuradores de Radicais Livres/farmacologia
Estresse Oxidativo/efeitos dos fármacos
Substâncias Protetoras/farmacologia
[Mh] Termos MeSH secundário: Trifosfato de Adenosina/metabolismo
Antipirina/farmacologia
Caspase 3/metabolismo
Células Epiteliais/citologia
Células Epiteliais/metabolismo
Epitélio Anterior/citologia
Epitélio Anterior/metabolismo
Seres Humanos
Potencial da Membrana Mitocondrial/efeitos dos fármacos
Mitocôndrias/efeitos dos fármacos
Mitocôndrias/metabolismo
Concentração Osmolar
Espécies Reativas de Oxigênio/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Free Radical Scavengers); 0 (Protective Agents); 0 (Reactive Oxygen Species); 8L70Q75FXE (Adenosine Triphosphate); EC 3.4.22.- (Caspase 3); S798V6YJRP (phenylmethylpyrazolone); T3CHA1B51H (Antipyrine)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170828
[Lr] Data última revisão:
170828
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170328
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0174437


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[PMID]:28277881
[Au] Autor:Martinez A; Palomo Ruiz MD; Perez DI; Gil C
[Ad] Endereço:a IPSBB Unit , Centro de Investigaciones Biologicas-CSIC , Madrid , Spain.
[Ti] Título:Drugs in clinical development for the treatment of amyotrophic lateral sclerosis.
[So] Source:Expert Opin Investig Drugs;26(4):403-414, 2017 Apr.
[Is] ISSN:1744-7658
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:INTRODUCTION: Amyotrophic Lateral Sclerosis (ALS) is a fatal motor neuron progressive disorder for which no treatment exists to date. However, there are other investigational drugs and therapies currently under clinical development may offer hope in the near future. Areas covered: We have reviewed all the ALS ongoing clinical trials (until November 2016) and collected in Clinicaltrials.gov or EudraCT. We have described them in a comprehensive way and have grouped them in the following sections: biomarkers, biological therapies, cell therapy, drug repurposing and new drugs. Expert opinion: Despite multiple obstacles that explain the absence of effective drugs for the treatment of ALS, joint efforts among patient's associations, public and private sectors have fueled innovative research in this field, resulting in several compounds that are in the late stages of clinical trials. Drug repositioning is also playing an important role, having achieved the approval of some orphan drug applications, in late phases of clinical development. Endaravone has been recently approved in Japan and is pending in USA.
[Mh] Termos MeSH primário: Esclerose Amiotrófica Lateral/tratamento farmacológico
Desenho de Drogas
Drogas em Investigação/uso terapêutico
[Mh] Termos MeSH secundário: Esclerose Amiotrófica Lateral/fisiopatologia
Animais
Antipirina/análogos & derivados
Antipirina/uso terapêutico
Terapia Biológica/métodos
Biomarcadores/metabolismo
Terapia Baseada em Transplante de Células e Tecidos/métodos
Reposicionamento de Medicamentos
Seres Humanos
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Biomarkers); 0 (Drugs, Investigational); S798V6YJRP (phenylmethylpyrazolone); T3CHA1B51H (Antipyrine)
[Em] Mês de entrada:1704
[Cu] Atualização por classe:170404
[Lr] Data última revisão:
170404
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170310
[St] Status:MEDLINE
[do] DOI:10.1080/13543784.2017.1302426


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[PMID]:28238613
[Au] Autor:Wu J; Ren J; Yao S; Wang J; Huang L; Zhou P; Yun D; Xu Q; Wu S; Wang Z; Qiu P
[Ad] Endereço:Chemical Biology Research Center, School of Pharmaceutical Sciences, Wenzhou Medical University, Wenzhou, Zhejiang 325035, China.
[Ti] Título:Novel antioxidants' synthesis and their anti-oxidative activity through activating Nrf2 signaling pathway.
[So] Source:Bioorg Med Chem Lett;27(7):1616-1619, 2017 04 01.
[Is] ISSN:1464-3405
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Novel structure compounds (WS) containing 3,4,5-trimethoxyphenyl and acyl pyrazole were designed and synthesized based combination principles. Among them, WS13 was screened out to possess desirable anti-oxidative activity in vitro. Cell survival assay and apoptosis experiment in H O induced PC12 cells injury model all showed that its cytoprotection exhibited a concentration-effect manner. WS13 at 10µM could remove ROS with equal effiency to edaravone. Further, it clearly activated Nrf2 nuclear translocation and upregulated GCLC mRNA transcription and protein expression in dose-dependent manner, and its cytoprotection was reversed by GCLC protein inhibitor. In total, WS13 with further promotion can serve as Nrf2-GCLC activator in anti-oxidative therapy.
[Mh] Termos MeSH primário: Antioxidantes/farmacologia
Fator 2 Relacionado a NF-E2/metabolismo
Substâncias Protetoras/farmacologia
[Mh] Termos MeSH secundário: Animais
Antioxidantes/síntese química
Antipirina/análogos & derivados
Antipirina/farmacologia
Apoptose/efeitos dos fármacos
Butionina Sulfoximina/farmacologia
Glutamato-Cisteína Ligase/antagonistas & inibidores
Glutamato-Cisteína Ligase/genética
Glutamato-Cisteína Ligase/metabolismo
Peróxido de Hidrogênio/farmacologia
Estresse Oxidativo/efeitos dos fármacos
Células PC12
Substâncias Protetoras/síntese química
Transporte Proteico
RNA Mensageiro/metabolismo
Ratos
Espécies Reativas de Oxigênio/metabolismo
Transdução de Sinais
Regulação para Cima
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Antioxidants); 0 (NF-E2-Related Factor 2); 0 (Nfe2l2 protein, rat); 0 (Protective Agents); 0 (RNA, Messenger); 0 (Reactive Oxygen Species); 5072-26-4 (Buthionine Sulfoximine); BBX060AN9V (Hydrogen Peroxide); EC 6.3.2.2 (Glutamate-Cysteine Ligase); EC 6.3.2.2. (GCLC protein, rat); S798V6YJRP (phenylmethylpyrazolone); T3CHA1B51H (Antipyrine)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:171124
[Lr] Data última revisão:
171124
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170228
[St] Status:MEDLINE


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[PMID]:28224430
[Au] Autor:Zhang DY; Kang SS; Zhang ZW; Wu R
[Ad] Endereço:Department of Plastic Surgery, Henan Provincial People's Hospital (Zhengzhou University People's Hospital), Zhengzhou, 450000, China.
[Ti] Título:Edaravone enhances the viability of ischemia/reperfusion flaps.
[So] Source:J Huazhong Univ Sci Technolog Med Sci;37(1):51-56, 2017 Feb.
[Is] ISSN:1672-0733
[Cp] País de publicação:China
[La] Idioma:eng
[Ab] Resumo:The purpose of the experiment was to study the efficacy of edaravone in enhancing flap viability after ischemia/reperfusion (IR) and its mechanism. Forty-eight adult male SD rats were randomly divided into 3 groups: control group (n=16), IR group (n=16), and edaravone-treated IR group (n=16). An island flap at left lower abdomen (6.0 cm×3.0 cm in size), fed by the superficial epigastric artery and vein, was created in each rat of all the three groups. The arterial blood flow of flaps in IR group and edaravone-treated IR group was blocked for 10 h, and then the blood perfusion was restored. From 15 min before reperfusion, rats in the edaravone-treated IR group were intraperitoneally injected with edaravone (10 mg/kg), once every 12 h, for 3 days. Rats in the IR group and control group were intraperitoneally injected with saline, with the same method and frequency as the rats in the edaravone-treated IR group. In IR group and edaravone-treated IR group, samples of flaps were harvested after reperfusion of the flaps for 24 h. In the control group, samples of flaps were harvested 34 h after creation of the flaps. The content of malondialdehyde (MDA) and activity of superoxide dismutase (SOD) were determined, and changes in organizational structure and infiltration of inflammatory cells were observed by hematoxylin-eosin (HE) staining, apoptotic cells of vascular wall were marked by terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling (TUNEL) assay, and the apoptotic rate of cells in vascular wall was calculated. The ultrastructural changes of vascular endothelial cells were observed by transmission electron microscopy (TEM). Seven days after the operation, we calculated the flap viability of each group, and marked vessels of flaps by immunohistochemical staining for calculating the average number of subcutaneous vessels. The results showed that the content of MDA, the number of multicore inflammatory cells and apoptotic rate of cells in vascular wall in the edaravone-treated IR group were significantly lower than those in the IR group. The activity of SOD, flap viability and average number of subcutaneous vessels in the edaravone-treated IR group were significantly higher than those in the IR group. All the differences were statistically significant. The ultrastructure injury of vascular endothelial cells in the edaravone-treated IR group was slighter than that in IR group. It was concluded that edaravone can significantly enhance IR flap viability and protect flap vessels, which is related to scavenging oxygen free radicals, reducing the consumption of SOD, reducing the extent of lipid peroxidation and inflammation, and protecting functional structure of vessels in the early stages of reperfusion.
[Mh] Termos MeSH primário: Antipirina/análogos & derivados
Sobrevivência de Enxerto/efeitos dos fármacos
Traumatismo por Reperfusão/prevenção & controle
Retalhos Cirúrgicos/irrigação sanguínea
Retalhos Cirúrgicos/patologia
[Mh] Termos MeSH secundário: Animais
Antipirina/administração & dosagem
Antipirina/farmacologia
Modelos Animais de Doenças
Precondicionamento Isquêmico/métodos
Masculino
Malondialdeído/metabolismo
Distribuição Aleatória
Ratos
Ratos Sprague-Dawley
Traumatismo por Reperfusão/patologia
Superóxido Dismutase/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
4Y8F71G49Q (Malondialdehyde); EC 1.15.1.1 (Superoxide Dismutase); S798V6YJRP (phenylmethylpyrazolone); T3CHA1B51H (Antipyrine)
[Em] Mês de entrada:1704
[Cu] Atualização por classe:171104
[Lr] Data última revisão:
171104
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170223
[St] Status:MEDLINE
[do] DOI:10.1007/s11596-017-1693-0



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