Researchers’ preliminary data indicate that, in airway epithelial cells, PI3Kγ primarily serves as a scaffold protein that anchors cAMP-degrading enzymes (PDE) to their activator, protein kinase A (PKA) and ultimately promotes cAMP clearance. A compound disrupting PI3Kγ scaffold function (Patent pending N°TO2014A001105) lowers PDE4 activity and enhances cAMP-mediated phosphorylation and activation of F508del CFTR. Intriguingly, this
molecule also promotes cAMP-mediated inactivation of leukocytes and cAMP-dependent relaxation of airway smooth muscle. Further results are expected in the extension project FFC#23/2015.