Intermittent BRAF inhibition in advanced BRAF mutated melanoma results of a phase II randomized trial

Nat Commun. 2021 Dec 1;12(1):7008. doi: 10.1038/s41467-021-26572-6.

Abstract

Combination treatment with BRAF (BRAFi) plus MEK inhibitors (MEKi) has demonstrated survival benefit in patients with advanced melanoma harboring activating BRAF mutations. Previous preclinical studies suggested that an intermittent dosing of these drugs could delay the emergence of resistance. Contrary to expectations, the first published phase 2 randomized study comparing continuous versus intermittent schedule of dabrafenib (BRAFi) plus trametinib (MEKi) demonstrated a detrimental effect of the "on-off" schedule. Here we report confirmatory data from the Phase II randomized open-label clinical trial comparing the antitumoral activity of the standard schedule versus an intermittent combination of vemurafenib (BRAFi) plus cobimetinib (MEKi) in advanced BRAF mutant melanoma patients (NCT02583516). The trial did not meet its primary endpoint of progression free survival (PFS) improvement. Our results show that the antitumor activity of the experimental intermittent schedule of vemurafenib plus cobimetinib is not superior to the standard continuous schedule. Detection of BRAF mutation in cell free tumor DNA has prognostic value for survival and its dynamics has an excellent correlation with clinical response, but not with progression. NGS analysis demonstrated de novo mutations in resistant cases.

Publication types

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

MeSH terms

  • Aged
  • Antineoplastic Agents / pharmacology*
  • Antineoplastic Agents / therapeutic use
  • Azetidines / pharmacology
  • Humans
  • Imidazoles / pharmacology
  • Melanoma / drug therapy*
  • Melanoma / genetics*
  • Mutation
  • Oximes / pharmacology
  • Piperidines / pharmacology
  • Protein Kinase Inhibitors / pharmacology*
  • Protein Kinase Inhibitors / therapeutic use
  • Proto-Oncogene Proteins B-raf / genetics*
  • Proto-Oncogene Proteins B-raf / metabolism*
  • Pyridones / pharmacology
  • Pyrimidinones / pharmacology
  • Vemurafenib / pharmacology

Substances

  • Antineoplastic Agents
  • Azetidines
  • Imidazoles
  • Oximes
  • Piperidines
  • Protein Kinase Inhibitors
  • Pyridones
  • Pyrimidinones
  • Vemurafenib
  • trametinib
  • BRAF protein, human
  • Proto-Oncogene Proteins B-raf
  • cobimetinib
  • dabrafenib

Associated data

  • ClinicalTrials.gov/NCT02583516