Recent progress in the identification of BRAF inhibitors as anti-cancer agents

Eur J Med Chem. 2014 Jan 24:72:170-205. doi: 10.1016/j.ejmech.2013.11.018. Epub 2013 Nov 27.

Abstract

The "RAS/BRAF/MEK/ERK" pathway has been associated with human cancers due to the frequent oncogenic mutations identified in its members. In particular, BRAF is mutated at high frequency in many cancers especially melanoma. This mutation leads to activation of the MAPK signaling pathway, inducing uncontrolled cell proliferation, and facilitating malignant transformation. All these facts make BRAF an ideal target for antitumor therapeutic development. Many BRAF inhibitors have been discovered during the last decade and most of them exhibit potent antitumor activity especially on tumors that harbor BRAF(V600E) mutations. Some of these compounds have entered clinical trials and displayed encouraged results. The present review highlights the progress in identification and development of BRAF inhibitors especially during the last five years.

Keywords: ADME; AKT/protein kinase B; Anti-cancer agents; BRAF; CR; CRD; ELISA; EMEA; ERK; European Medicine Agency; FDA; Food and Drug Administration; GTP; HCC; IV; Inhibitors; JAK; Janus kinase; Lck; MAPK; MD; NTRKs; PDGFR; PET; PK; PKB; QM/MM; RAF; RAS-binding domain; RBD; RCC; RTKs; SCID; SRB; STKs; Src; VEGFR; abelson murine leukemia viral oncogene homolog 1; abl; absorption, distribution, metabolism and excretion; conserved regions; cysteine-rich domain, DFG, D594, F595, and G596; enzyme-linked immunosorbent assay; extracellular signal-regulated kinase; guanosine triphosphate; hepatocellular carcinoma; intravenous; lymphocyte-specific protein tyrosine kinase; mitogen-activated protein kinase; mitogen-activated protein kinase 14; molecular dynamics; non-receptor tyrosine kinases; p38α; pharmacokinetic; platelet-derived growth factor receptor; positron emission tomography; proto-oncogene tyrosine-protein kinase; quantum mechanics/molecular mechanics; rapidly growing fibrosarcoma; receptor tyrosine kinases; renal cell carcinoma; serine–threonine kinases; severe combined immunodeficiency; sulforhodamine B assay; vascular endothelial growth factor receptor.

Publication types

  • Review

MeSH terms

  • Antineoplastic Agents / chemistry
  • Antineoplastic Agents / pharmacology*
  • Cell Proliferation / drug effects
  • Humans
  • Models, Molecular
  • Molecular Structure
  • Neoplasms / drug therapy*
  • Neoplasms / enzymology
  • Neoplasms / pathology
  • Protein Kinase Inhibitors / chemistry
  • Protein Kinase Inhibitors / pharmacology*
  • Proto-Oncogene Mas
  • Proto-Oncogene Proteins B-raf / antagonists & inhibitors*
  • Proto-Oncogene Proteins B-raf / genetics
  • Proto-Oncogene Proteins B-raf / metabolism
  • Structure-Activity Relationship

Substances

  • Antineoplastic Agents
  • MAS1 protein, human
  • Protein Kinase Inhibitors
  • Proto-Oncogene Mas
  • Proto-Oncogene Proteins B-raf