Phase II Studies with Refametinib or Refametinib plus Sorafenib in Patients with RAS-Mutated Hepatocellular Carcinoma

Clin Cancer Res. 2018 Oct 1;24(19):4650-4661. doi: 10.1158/1078-0432.CCR-17-3588. Epub 2018 Jun 27.

Abstract

Purpose: Refametinib, an oral MEK inhibitor, has demonstrated antitumor activity in combination with sorafenib in patients with RAS-mutated hepatocellular carcinoma (HCC). Two phase II studies evaluated the efficacy of refametinib monotherapy and refametinib plus sorafenib in patients with RAS-mutant unresectable or metastatic HCC.Patients and Methods: Eligible patients with RAS mutations of cell-free circulating tumor DNA (ctDNA) determined by beads, emulsion, amplification, and magnetics technology received twice-daily refametinib 50 mg ± sorafenib 400 mg. Potential biomarkers were assessed in ctDNA via next-generation sequencing (NGS).Results: Of 1,318 patients screened, 59 (4.4%) had a RAS mutation, of whom 16 received refametinib and 16 received refametinib plus sorafenib. With refametinib monotherapy, the objective response rate (ORR) was 0%, the disease control rate (DCR) was 56.3%, overall survival (OS) was 5.8 months, and progression-free survival (PFS) was 1.9 months. With refametinib plus sorafenib, the ORR was 6.3%, the DCR was 43.8%, OS was 12.7 months, and PFS was 1.5 months. In both studies, time to progression was 2.8 months. Treatment-emergent toxicities included fatigue, hypertension, and acneiform rash. Twenty-seven patients had ctDNA samples available for NGS. The most frequently detected mutations were in TERT (63.0%), TP53 (48.1%), and β-catenin (CTNNB1; 37.0%).Conclusions: Prospective testing for RAS family mutations using ctDNA was a feasible, noninvasive approach for large-scale mutational testing in patients with HCC. A median OS of 12.7 months with refametinib plus sorafenib in this small population of RAS-mutant patients may indicate a synergistic effect between sorafenib and refametinib-this preliminary finding should be further explored. Clin Cancer Res; 24(19); 4650-61. ©2018 AACR.

Publication types

  • Clinical Trial, Phase II
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adult
  • Aged
  • Antineoplastic Combined Chemotherapy Protocols / administration & dosage
  • Carcinoma, Hepatocellular / blood
  • Carcinoma, Hepatocellular / drug therapy*
  • Carcinoma, Hepatocellular / genetics
  • Carcinoma, Hepatocellular / pathology
  • Circulating Tumor DNA / blood
  • Diphenylamine / administration & dosage
  • Diphenylamine / analogs & derivatives
  • Disease-Free Survival
  • Female
  • Humans
  • Liver Neoplasms / blood
  • Liver Neoplasms / drug therapy*
  • Liver Neoplasms / genetics
  • Liver Neoplasms / pathology
  • MAP Kinase Kinase Kinases / antagonists & inhibitors
  • Male
  • Middle Aged
  • Mutation
  • Protein Kinase Inhibitors / administration & dosage
  • Sorafenib / administration & dosage
  • Sulfonamides / administration & dosage
  • Telomerase / genetics*
  • Tumor Suppressor Protein p53 / genetics*
  • beta Catenin / genetics*
  • ras Proteins / genetics

Substances

  • CTNNB1 protein, human
  • Circulating Tumor DNA
  • N-(3,4-difluoro-2-(2-fluoro-4-iodophenylamino)-6-methoxyphenyl)-1-(2,3-dihydroxypropyl)cyclopropane-1-sulfonamide
  • Protein Kinase Inhibitors
  • Sulfonamides
  • TP53 protein, human
  • Tumor Suppressor Protein p53
  • beta Catenin
  • Diphenylamine
  • Sorafenib
  • MAP Kinase Kinase Kinases
  • TERT protein, human
  • Telomerase
  • ras Proteins