Ivacaftor affects the susceptibility of standard-of-care drugs used to treat Mycobacterium abscessus lung disease.

Patients with cystic fibrosis have dysfunctional cystic fibrosis transmembrane conductance regulator (CFTR), and this predisposes them to nontuberculous mycobacteria (NTM), including Mycobacterium abscessus (MAB), infection. We found that one of the CFTR modulators, ivacaftor, kills MAB in a concentration-dependent manner, with killing efficacy comparable to amikacin and imipenem, drugs in guideline-based regimens. Using clinical isolates of MAB, amikacin 1/4× MIC concentration combined with ivacaftor killed 2.67 log10 CFU/mL MAB.