Dabrafenib

Radhika Kainthla, Kevin B. Kim, Gerald S. Falchook

Research output: Contribution to journalArticle

3 Citations (Scopus)

Abstract

Dabrafenib was developed as a highly specific reversible inhibitor of V600-mutant BRAF kinase, an oncogenic mutation driving proliferation in many different types of aggressive tumors. Metastatic melanoma has a high prevalence of V600-mutant BRAF, and clinical trials showed that dabrafenib improved response rates and median progression-free survival in patients with V600E BRAF mutations, including those with brain metastasis. Preliminary results suggest that dabrafenib may also have some role in non-melanoma V600-mutant solid tumors; however, more studies are needed. With a welltolerated toxicity profile and few drug interactions, dabrafenib is effective as a monotherapy; however, resistance eventually develops in most patients after persistent exposure to the drug. Current research focuses on combination strategies with dabrafenib to not only improve response rates but also overcome resistance.

Original languageEnglish (US)
Pages (from-to)227-240
Number of pages14
JournalRecent Results in Cancer Research
Volume201
DOIs
StatePublished - Jan 1 2014
Externally publishedYes

Fingerprint

Proto-Oncogene Proteins B-raf
Mutation
Drug Interactions
Disease-Free Survival
Melanoma
Neoplasms
dabrafenib
Clinical Trials
Neoplasm Metastasis
Brain
Research
Pharmaceutical Preparations

ASJC Scopus subject areas

  • Oncology
  • Cancer Research

Cite this

Dabrafenib. / Kainthla, Radhika; Kim, Kevin B.; Falchook, Gerald S.

In: Recent Results in Cancer Research, Vol. 201, 01.01.2014, p. 227-240.

Research output: Contribution to journalArticle

Kainthla, Radhika ; Kim, Kevin B. ; Falchook, Gerald S. / Dabrafenib. In: Recent Results in Cancer Research. 2014 ; Vol. 201. pp. 227-240.
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