, gilteritinib inhibited H2228/Al cell growth, induced apoptosis and reduced ALK protein levels. Co‑culture and rescue experiments suggested the mechanism involved inhibiting PD‑L1 and CD8 co‑expression, corroborated by animal experiments. Gilteritinib can overcome alectinib resistance and inhibit PD‑L1 and CD8 co‑expression in ALK‑rearranged NSCLC, providing a new therapeutic strategy.
Guo et al. (Tue,) studied this question.
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