F508del is a mutation that causes the CFTR protein to misfold and cells destroy such proteins soon after they are made;<unk>  acts as a chaperone during protein folding and increases the number of CFTR proteins that are trafficked to the cell surface. Ivacaftor is a potentiator of CFTR that is already at the cell surface, increasing the probability that the defective channel will be open and allow chloride ions to pass through the channel pore. The two drugs have synergistic effects.
Lumacaftor/ivacaftor
Elexacaftor/tezacaftor/ivacaftor
Beclometasone/formoterol/glycopyrronium bromide
Mometasone/formoterol
Fluticasone/salmeterol
Beclometasone/formoterol
Lifitegrast
Ivacaftor