On the contrary, there was a marked increase in MIC to.8 mM for M. bovis BCG transformants containing all three inserts encompassing qcrB. At 166MIC, we found ample growth from all three inserts, including pMV261::qcrB, despite the reported finding that QcrB was only expressed to 10% efficiency if lacking functional QcrC in overexpression vectors. This result clearly confirms QcrB as the target of IP 3 and the other IP compounds: increased expression levels of the IP target enable higher concentrations of IP to enter the cell and bind QcrB without a fatal impact on cell survival. This study has revealed the IP inhibitor family as a promising anti-tubercular agent, targeting an essential component of the electron transport chain, QcrB. Due to the nature of the target, it is conceivable that the IP compounds could target both active and Doxorubicin latent phases of TB infection, an important requirement of future anti-tubercular agents. In most cultured cell models and native epithelia, a small portion of the F508del protein can escape the quality control system of the ER, and subsequently undergo complex glycosylation in the Golgi compartment and transfer to the apical membrane of epithelial cells. The F508del protein at the cell surface is active as a chloride channel, though with a strongly reduced open probability and considerably higher turnover rate as compared to wild type CFTR. The SU5416 instability of rescued F508del CFTR was attributed to unfolding and subsequent ubiquitination, endocytosis, and lysosomal degradation by a peripheral protein QC system sharing multiple chaperones and co-chaperones with the QC in the ER. Attempts to correct the F508del CFTR allelespecific phenotype are currently focussed on the selection of compounds that overcome the inefficient folding of the mutant protein, or enhance the CFTR chloride channel activity. Small molecule correctors may also act as pharmacological chaperones and enhance the cellsurface stability of F508del-CFTR. Partial rescue of the human F508del CFTR protein has been demonstrated in cell culture using different strategies. Initially, restoration of F508del CFTR processing was accomplished by low temperature incubation. Subsequently, competition with truncated CFTR constructs, chemical chaperones, transcriptional regulators, pharmacological chaperones or modification of available lead compounds. Most of these studies have been performed with primary or immortalised human airway cells in vitro. Recent studies showed that the relative efficacy of different types of correctors depends on the cell type and experimental context. This limits the predictive value of in vitro data for clinical applications assays and stresses the importance of choosing models that reflect the in vivo situation. Prior to expensive and potentially harmful clinical trials, testing of a promising candidate in the context of a fully differentiated organ is advisable.