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Unité de recherche
INNOSUISSE
Numéro de projet
9148.2;13 PFLS-LS
Titre du projet
Development of a novel chemical entity to treat fibrocontractive diseases
Titre du projet anglais
Development of a novel chemical entity to treat fibrocontractive diseases

Textes relatifs à ce projet

 AllemandFrançaisItalienAnglais
Description succincte
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Résumé des résultats (Abstract)
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Textes saisis


CatégorieTexte
Description succincte
(Anglais)
Development of a novel chemical entity to treat fibrocontractive diseases
Description succincte
(Français)
Development of a novel chemical entity to treat fibrocontractive diseases
Résumé des résultats (Abstract)
(Anglais)
Hypertrophic wounds (e.g. burns), fibromatosis (e.g. Dupuytren's disease) and fibrotic diseases (e.g. lung fibrosis) are characterized by pathological contraction caused by myofibroblast contraction, being promoted by á-smooth muscle actin (á-SMA) in stress fibers. It has been shown that the administration of the á-SMAspecific N-terminal sequence Ac-EEED as tetrapeptide leads to the removal of á-SMA from stress fibers, reverses myofibroblasts into non-fibrogenic fibroblasts and reduces wound contraction. However, the short lifetime of the peptide and problems linked with the delivery of the peptide have prevented from any clinical development until now. Capitalizing on the experience of ArisGen, a company specialized on peptide delivery, we want to generate a new derivatized Ac-EEED peptido-mimetic as therapeutically active compound and test novel peptide delivery technology, proprietary of ArisGen a to allow topically and systemically application to inhibit tissue contractures.
Résumé des résultats (Abstract)
(Français)
Hypertrophic wounds (e.g. burns), fibromatosis (e.g. Dupuytren's disease) and fibrotic diseases (e.g. lung fibrosis) are characterized by pathological contraction caused by myofibroblast contraction, being promoted by á-smooth muscle actin (á-SMA) in stress fibers. It has been shown that the administration of the á-SMAspecific N-terminal sequence Ac-EEED as tetrapeptide leads to the removal of á-SMA from stress fibers, reverses myofibroblasts into non-fibrogenic fibroblasts and reduces wound contraction. However, the short lifetime of the peptide and problems linked with the delivery of the peptide have prevented from any clinical development until now. Capitalizing on the experience of ArisGen, a company specialized on peptide delivery, we want to generate a new derivatized Ac-EEED peptido-mimetic as therapeutically active compound and test novel peptide delivery technology, proprietary of ArisGen a to allow topically and systemically application to inhibit tissue contractures.