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MEGFIB

Financiado

Noncoding RNA MEG3 inhibitor for Heart Failure Treatment

Cardiac fibrosis is a hallmark of and mechanistically involved in heart failure; a disease will high clinical unmet need and fundamental socioeconomic importance. Specific treatments of cardiac fibrosis are lacking. RNAs that do n... ver más

31/12/2021

MHH

150K€

Presupuesto del proyecto: 150K€

Líder del proyecto

MEDIZINISCHE HOCHSCHULE HANNOVER No se ha especificado una descripción o un objeto social para esta compañía.

TRL 4-5

Ver 2 Participantes

Financiación concedida El organismo H2020 notifico la concesión del proyecto el día 2021-12-31

ERC-2019-POC: ERC Proof of Concept Grant

I+D

Cerrada hace 5 años

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Información adicional privada

No hay información privada compartida para este proyecto. Habla con el coordinador.

2 Participantes

MHH

150.00K€ | Lider

RC Electrónica

66.00K€ | Participante

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Duración del proyecto: 20 meses Fecha Inicio: 2020-04-15
Fecha Fin: 2021-12-31

Líder del proyecto

MEDIZINISCHE HOCHSCHULE HANNOVER No se ha especificado una descripción o un objeto social para esta compañía.

TRL 4-5

Presupuesto del proyecto 150K€

Descripción del proyecto Cardiac fibrosis is a hallmark of and mechanistically involved in heart failure; a disease will high clinical unmet need and fundamental socioeconomic importance. Specific treatments of cardiac fibrosis are lacking. RNAs that do not code for proteins comprise a large portion of the human genome. These so-called noncoding RNAs are emerging as important players in disease pathogenesis, yet their functional roles are ill understood. Our group currently pioneered first clinical testings on noncoding RNA inhibitors in heart failure patients showing the enormous clinical translational potential of such next-generation therapeutics. We now aim to develop a new approach to treat selected heart failure patients, which show increased signs of cardiac fibrosis. Within the ERC grant LONGHEART we have identified a lncRNA meg3 to be a novel and innovative target in heart failure pathologies with fibrosis (Circ Res. 2017 Aug 18;121(5):575-583; Fig. 1). Importantly meg3 is well conserved between rodents and humans allowing translational development. Oligonucleotide-mediated silencing of Meg3 in human cardiac fibroblasts and in vivo in mice resulted in decreased cardiac fibrosis and improved diastolic performance of the heart. Within MEGFIB, we now aim to advance these valuable research results on meg3-based improvements of cardiac fibrosis in mice towards commercial proof-of-concept. Important next steps are a) translation of the efficacy to human cells and tissues and b) sophisticated market analysis, c) IP strategy development and d) business development activities to maximize the value of the projects’ results. The outcome of our activities will be consolidated into a business plan for presenting our proposition to strategic partners, such as Cardior Pharmaceuticals or venture capitalists (VCs). We are proposing a unique RNA-based approach that offers a new opportunity to revolutionize medical practice, improve patient care and will reduce costs in the heart failure care.

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