Refametinib

Description	in vitro: BAY 86-9766 exhibited potent antiproliferative activity in HCC cell lines with half-maximal inhibitory concentration values ranging from 33 to 762 nM. BAY 86-9766 was strongly synergistic with sorafenib in suppressing tumor cell proliferation and inhibiting phosphorylation of the extracellular signal-regulated kinase (ERK). in vivo: BAY 86-9766 prolonged survival in Hep3B xenografts, murine Hepa129 allografts, and MH3924A rat allografts. Additionally, tumor growth, ascites formation, and serum alpha-fetoprotein levels were reduced [1]. In a phase I/II study of patients with advanced solid tumors, refametinib was well tolerated at doses 100 mg daily. Rash was the most common TEAE. Subsequently, a phase II study enrolled seventy patients to evaluate refametinib in combination with sorafenib as first-line treatment for unresectable hepatocellular carcinoma (HCC). Of sixty-five patients analyzed for efficacy per protocol, three (5%) had PR, and the median time-to-progression was
Pathways	MAPK Pathway
Targets	MEK/ERK

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