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We generated recombinant cystic fibrosis transmembrane conductance regulator (CFTR) mutants, containing either the DeltaF508 deletion or other mutations in the NBD2 domain, and characterized the function of the mutant CFTRs. We found that the mutant CFTRs were markedly less thermostable than wild-type CFTR, suggesting that this is a major characteristic of the DeltaF508 mutation. Phenotypic correction of the DeltaF508 mutant by a small-molecule CFTR corrector, VX-809, was associated with a much more marked increase in the thermostability of the mutant CFTR. Although VX-809 is currently being studied in phase I clinical trials for the treatment of cystic fibrosis, the increase in thermostability of DeltaF508 mutant CFTR makes it a potential candidate for such trials.Q:
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