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Management of NASH should focus on the restitution of metabolic derangements and halting inflammatory, fibrogenic, and carcinogenic pathways

Hyperoside (HY) inhibited the viability of human non-small cell lung cancer A549 cells in a time- and dose-dependent manner and induced apoptosis via the p38 MAPK- and JNK-induced mitochondrial death pathway (57)

Moreover, SYP-14288-resistant mutant X19-7 significantly enhanced SYP-14288 metabolism on M1, and M1 accumulation in X19-7 might account for the decrease of the sensitivity to SYP-14288, whereas M2 and M3 were less important in the resistance