Pharmacological inhibition of STAT1 enhances iPSC-PLT production under turbulent flow conditions. (A) Chemical structures of fludarabine and flavopiridol, the 2 established inhibitors for STAT1 phosphorylation. (B) Dose optimization on iPSC-PLT production of fludarabine (0 to ∼5 μM) and flavopiridol (0 to ∼100 nM). (C) iPSC-PLT generation by imMKCLs (clone 7) in the absence and presence of fludarabine (1 μM) or flavopiridol (10 nM) under static or turbulent flow conditions. (D) Representative flow cytometry plots of iPSC-PLTs generated in the absence and presence of fludarabine (1 μM) or flavopiridol (10 nM) in static or turbulent flow conditions. CD41⁺CD42b⁺ platelets were identified from a platelet-sized gate. (E) Fludarabine (1 μM) or flavopiridol (10 nM) treatments elevated let-7a-5p expression. (F) Flavopiridol (10 nM) treatment reduced mRNA expression of representative immune-related genes in imMKCLs at the maturation stage. Data are expressed as the mean ± SEM from 4 to 5 independent experiments. Statistical significance was assed using 1-way analysis of variance or unpaired 2-tailed Student t tests. DMSO, dimethyl sulfoxide.