PSORIASIS-TREAT

Directed Evolution of Soluble IL-17A Receptor for Psoriasis Therapeutics

Coordinatore	BEN-GURION UNIVERSITY OF THE NEGEV    more Spiacenti, non ci sono informazioni su questo coordinatore. Contattare Fabio per maggiori infomrazioni, grazie.
Nazionalità Coordinatore	Israel [IL]
Totale costo	167˙939 €
EC contributo	149˙746 €
Programma	FP7-IDEAS-ERC Specific programme: "Ideas" implementing the Seventh Framework Programme of the European Community for research, technological development and demonstration activities (2007 to 2013)
Code Call	ERC-2013-PoC
Funding Scheme	CSA-SA(POC)
Anno di inizio	2014
Periodo (anno-mese-giorno)	2014-01-01   -   2015-06-30

 Partecipanti

#	participant	country	role	EC contrib. [€]
1	BEN-GURION UNIVERSITY OF THE NEGEV  Organization address address: Office of the President - Main Campus city: BEER SHEVA postcode: 84105 contact info Titolo: Ms. Nome: Daphna Cognome: Tripto Email: send email Telefono: 97286472443 Fax: 97286472930	IL (BEER SHEVA)	hostInstitution	149˙746.00

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 Obiettivo del progetto (Objective)

'Protein therapeutics has increased dramatically over the last two decades and currently includes more than 130 therapeutic proteins in almost all fields of medicine. However, many proteins are not suitable for therapeutic application due to the lack of sufficient in vivo stability and biological efficacy. Thus, engineering of existing proteins for improved affinity and stability will significantly increase their potential for therapeutic applications. In recent years, the cytokine interleukin 17A (IL-17A) was identified as an important pro-inflammatory protein that plays an essential role in the progression of several autoimmune diseases including psoriasis, rheumatoid arthritis and inflammatory bowel disease. Thus, IL-17A is a promising drug target, and blocking its interactions with the endogenous IL-17RA receptor may constitute an important strategy for the treatment of common autoimmune diseases. We have recently applied protein engineering to generate decoy IL-17RA mutants with improved binding affinity and stability relative to the native soluble receptor. These variants showed promising results in inhibiting psoriasis plaque formation in a human psoriasis mouse model. Here, I propose to further develop the engineered IL-17RA for future pre-clinical and clinical development and pave the way for its commercialization. I propose to perform final lead optimization of the engineered IL-17RA variants by reducing the number of mutations while maintaining the improved characteristics of the engineered receptor. In parallel, I intend to perform detailed intellectual property (IP) and market analysis for identifying the ideal partner to promote the commercialization of the engineered IL-17RA. Further development of engineered IL-17RA and its commercialization will increase our chances for obtaining a highly efficient and a more affordable therapeutic approach for psoriasis and potentially for other common autoimmune diseases.'