ALUNBRIG® (brigatinib): A POTENT ALK INHIBITOR1

ALUNBRIG Mechanism of Action (MOA)

  • A tyrosine kinase inhibitor with in vitro activity at clinically achievable concentrations against multiple kinases including ALK (IC50: 14 nM), ROS1 (IC50: 18 nM), insulin-like growth factor-1 receptor (IGF-1R) (IC50: 148 nM), and FLT-3 (IC50: 158 nM) as well as EGFR deletion and point mutations1
  • Inhibited autophosphorylation of ALK and ALK-mediated phosphorylation of the downstream signaling proteins STAT3, AKT, ERK1/2, and S6 in in vitro and in vivo assays
  • ALUNBRIG inhibited the in vitro proliferation of cell lines expressing EML4-ALK and NPM-ALK fusion proteins
  • Demonstrated dose-dependent inhibition of EML4-ALK+ NSCLC xenograft growth in mice
  • At clinically achievable concentrations (≤500 nM), brigatinib inhibited the in vitro viability of cells expressing EML4-ALK and 17 mutant forms associated with resistance to ALK inhibitors including crizotinib, as well as EGFR-Del (E746-A750), ROS1-L2026M, FLT3-F691L, and FLT3-D835Y
  • Brigatinib exhibited in vivo antitumor activity against 4 mutant forms of EML4-ALK, including G1202R and L1196M mutants identified in NSCLC tumors in patients who had progressed on crizotinib. See more
Image reused from Zhang S et al. Clinical Cancer Research, 2016;22(22):5527-5538, with permission from AACR.

ALUNBRIG Demonstrated In Vivo Antitumor Activity in the CNS

  • ALUNBRIG reduced tumor burden and prolonged survival in mice with an ALK-driven tumor cell line implanted intracranially

AACR, American Association for Cancer Research; ALK, anaplastic lymphoma kinase; CNS, central nervous system; NSCLC, non-small cell lung cancer.

 


 

References

1. Zhang S, Anjum R, Squillace R, et al. Clin Cancer Res. 2016;22(22):5527-5538. 2. Zhang S, Anjum R, Squillace R, et al. Supplementary figures. Clin Cancer Res. 2016;22(22):5527-5538. doi:10.1158/1078-0432.CCR-16-0569.

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In Vitro: ALUNBRIG Inhibited 17
ALK-Inhibitor—Resistant Mutations1,2

ALUNBRIG exhibited in vivo antitumor activity against 4 mutant forms of EML4-ALK, including the G1202R and L1196M mutants identified in NSCLC tumors in patients who had progressed on crizotinib.


 
 

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