The challenge of this project is clearly 1) to propose a new pharmacological target for CF therapy and 2) to gain insights into and to better understand the mechanism of action of iminosugars-based correctors in order to generate more potent and selective correctors. Our models for misfolded proteins and human diseases include F508del-CFTR channel responsible for cystic fibrosis. The originality and novelty of this study is based first on the exploration of a new pharmaceutical target, the mannosidases of the ER, to better understand how our chemical chaperone is activating F508del-CFTR. The second novel aspect is related to the originality of the corrector structures which are based on multivalent systems displaying a controlled number of copies of mannosidase inhibitors. These compounds will be efficiently synthesized from various scaffolds by way of “click chemistry”.