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However, the upregulation of MET expression in HCC presents a challenge: Oxidative DNA damage activates MET, which interacts with and phosphorylates PARP-1 at tyrosine 907, thereby limiting the effectiveness of PARP-1 inhibitors in HCC (109)

Biochemical Pharmacology, 2011

The compound works through a unique mechanism involving G-actin sequestration, which essentially maintains a reservoir of cellular building blocks ready for rapid deployment when tissue repair is needed