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. 2020 Jul 24;75(9):754–763. doi: 10.1136/thoraxjnl-2019-214000

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© Author(s) (or their employer(s)) 2020. Re-use permitted under CC BY-NC. No commercial re-use. See rights and permissions. Published by BMJ.

This is an open access article distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited, appropriate credit is given, any changes made indicated, and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/.

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Nintedanib inhibits ckit activation. (A) Nintedanib inhibits phosphorylation of ckit induced by 10 min stimulation with 4 nM rhSCF. IC₅₀: 2.5 nM vs 13.3 nM for anti-SCF and nintedanib, respectively. (B) Nintedanib inhibits mast cell (MC) proliferation induced by stimulation of MCs with 4 nM rhSCF for 3 days. (C) Nintedanib inhibits CCL2 release induced by stimulation of MCs with 4 nM rhSCF for 3 days. Data are plotted as mean (SE) of 3 separate experiments. DMSO was used as a vehicle control and anti-SCF pAb was included as a positive control. CBMC, cord blood–derived mast cell; SCF, stem cell factor.