Leukemia Drug Has Potential to Treat Asthma

The KIT inhibitor, imatinib, reduced airway hyperresponsiveness and the production of mast-cells, according to a recent study. The findings from this proof-of-principle study suggests that imatinib could possibly be used for the treatment of severe and poorly controlled asthma.

Mast cells present in the airways of patient with severe asthma are associated with poor quality of life and inadequately controlled asthma. They require stem cell factors and KIT receptors to maintain homeostasis, leading the researchers to hypothesize that the KIT inhibitor imatinib could possible reduce mast-cell numbers in patients with asthma and improve symptoms.
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The randomized, double-blind, placebo-controlled trial included 62 patients with poorly controlled severe asthma and airway hyperresponsiveness despite receiving maximal medical therapy. Patients received either imatinib or placebo for 24 weeks. The change in airway hyperresponsiveness was assessed as the primary end-point, and patients also underwent bronchoscopy.

Overall, imatinib reduced airway hyperresponsiveness to a greater extent than the placebo, as well as greatly reduced serum tryptase levels. Airway mast-cell counts declined in both the placebo and imatinib groups.

Methacholine PC₂₀ increased by a mean of 1.73±0.60 doubling doses at 6 months in participants in the imatinib group compared with 1.07±0.60 doubling doses in participants in the placebo group.

However, participants in the imatinib group experienced muscle cramps and hypophosphatemia more than participants in the placebo group.

“In patients with severe asthma, imatinib decreased airway hyperresponsiveness, mast-cell counts, and tryptase release,” the researchers concluded. “These results suggest that KIT-dependent processes and mast cells contribute to the pathobiologic basis of severe asthma.”

—Melissa Weiss

Reference:

Cahill KN, Katz HR, Cui J, et al. KIT inhibition by imatinib in patients with severe refractory asthma [published online May 18, 2017]. N Engl J Med. doi:1056/NEJMoa1613125.