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• W2170039319 abstract "The cystic fibrosis transmembrane conductance regulator (CFTR) is a cAMP-regulated chloride channel localized primarily at the apical surfaces of epithelial cells lining airway, gut and exocrine glands, where it is responsible for transepithelial salt and water transport. Several human diseases are associated with an altered channel function of CFTR. Cystic fibrosis (CF) is caused by the loss or dysfunction of CFTR-channel activity resulting from the mutations on the gene; whereas enterotoxin-induced secretory diarrheas are caused by the hyperactivation of CFTR channel function. CFTR is a validated target for drug development to treat these diseases. Significant progress has been made in developing CFTR modulator therapy by means of high-throughput screening followed by hit-to-lead optimization. Several oral administrated investigational drugs are currently being evaluated in clinical trials for CF. Also importantly, new ideas and methodologies are emerging. Targeting CFTR-containing macromolecular complexes is one such novel approach." @default.
• W2170039319 created "2016-06-24" @default.
• W2170039319 creator A5037988546 @default.
• W2170039319 creator A5045543880 @default.
• W2170039319 creator A5069690311 @default.
• W2170039319 date "2012-03-01" @default.
• W2170039319 modified "2023-09-27" @default.
• W2170039319 title "Recent advances and new perspectives in targeting CFTR for therapy of cystic fibrosis and enterotoxin-induced secretory diarrheas" @default.
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• W2170039319 doi "https://doi.org/10.4155/fmc.12.1" @default.
• W2170039319 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/3320517" @default.
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