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. 2019 Jan 30;176(6):773–786. doi: 10.1111/bph.14562

Figure 2.

Figure 2

Class II kinase inhibitors do not affect the propensity for SOICR. HEK293 cells stably expressing RyR2 were loaded with fluo‐4 in KRH buffer. Cells were superfused with KRH containing 0, 0.1, 0.2, 0.3, 0.5 or 1 mM Ca2+. At the end of each experiment, cells were perfused with 20 mM caffeine. Representative fluo‐4 traces presented from cells treated with 1, 3 or 10 μM ponatinib (A) or nilotinib (C). (B) The fraction of cells experiencing SOICR at each [Ca2+]o when treated with vehicle, 1, 3 or 10 μM ponatinib. (D) The fraction of cells experiencing SOICR at each [Ca2+]o when treated with vehicle, 1, 3 or 10 μM nilotinib. Data shown are mean ± SEM. For ponatinib, n = 16 (vehicle), 8 (1 μM), 9 (3 μM) or 12 (10 μM) independent experiments. For nilotinib, n = 16 (vehicle), 12 (1 μM), 8 (3 μM) or 10 (10 μM) independent experiments.