7th of June 2011, Source: PR Newswire
MOUNTAIN VIEW, Calif., June 8, 2011 /PRNewswire/ -- Edison Pharmaceuticals, Inc. announced today that the U.S. Food and Drug Administration (FDA) has allowed an Expanded Access program to provide EPI-743 to seriously ill patients diagnosed with inherited respiratory chain diseases of the mitochondria. read more
Edison Pharmaceuticals élargit l'accès à EPI-743 pour les maladies mitochondriales
MOUNTAIN VIEW, Californie, June 8, 2011 /PRNewswire/ --
- La FDA autorise l'utilisation d'un nouveau médicament expérimental pour les cas menaçant le pronostic vital
Edison Pharmaceuticals, Inc. a aujourd'hui annoncé que la "Food and Drug Administration" américaine (la FDA) a autorisé un programme d'accès élargi pour offrir EPI-743 aux patients gravement malades ayant reçu un diagnostic de maladies héréditaires de la chaîne respiratoire mitochondriale. Les patients dont la maladie a été génétiquement confirmée comme ceux qui répondent à certains critères cliniques, en l'absence de confirmation génétique, sont tous éligibles. Lire plus.......
Edison Pharmaceuticals sorgt für erweiterten Zugang zu EPI-743 für mitochondriale Erkrankungen
MOUNTAIN VIEW, Kalifornien, June 8, 2011 /PRNewswire/ --
- FDA genehmigt Anwendung von Medikament in klinischer Testphase (Investigational New Drug) bei lebensbedrohlichen Befunden
Edison Pharmaceuticals, Inc. gab heute bekannt, dass die amerikanische Zulassungsbehörde für Lebens- und Arzneimittel, die US Food and Drug Administration (FDA), ein sogenanntes Expanded-Access-Programm genehmigt hat, durch das EPI-743 an schwerkranke Patienten mit diagnostizierter Störung der Atmungskette aufgrund mitochondrialer Erbkrankheiten verabreicht werden darf. Darunter fallen sowohl Patienten mit genetisch bestätigter Krankheit als auch Patienten, die bei fehlender genetischer Bestätigung spezifische klinische Kriterien erfüllen. Lesen Sie mehr ...
Wednesday, June 8, 2011
Differential Expression of PGC-1α and Metabolic Sensors Suggest Age-Dependent Induction of Mitochondrial Biogenesis in Friedreich Ataxia Fibroblasts
2011 PLoS ONE 6(6): e20666. doi:10.1371/journal.pone.0020666, OPEN ACCESS
García-Giménez JL, Gimeno A, Gonzalez-Cabo P, Dasí F, Bolinches-Amorós A, et al.
The induction of mitochondrial biogenesis in FRDA may be a consequence of the mitochondrial impairment associated with disease evolution. The increase of ROS and the involvement of the oxidative phosphorylation may be an early event in the cell pathophysiology of frataxin deficiency, whereas increase of mitochondriogenic response might be a later phenomenon associated to the individual age and natural history of the disease, being more evident as the patient age increases and disease evolves. This is a possible explanation of heart disease in FRDA.
FULL TEXT PDF
García-Giménez JL, Gimeno A, Gonzalez-Cabo P, Dasí F, Bolinches-Amorós A, et al.
The induction of mitochondrial biogenesis in FRDA may be a consequence of the mitochondrial impairment associated with disease evolution. The increase of ROS and the involvement of the oxidative phosphorylation may be an early event in the cell pathophysiology of frataxin deficiency, whereas increase of mitochondriogenic response might be a later phenomenon associated to the individual age and natural history of the disease, being more evident as the patient age increases and disease evolves. This is a possible explanation of heart disease in FRDA.
FULL TEXT PDF
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