nvp-tae684 and Lymphoma--Large-B-Cell--Diffuse

nvp-tae684 has been researched along with Lymphoma--Large-B-Cell--Diffuse* in 1 studies

Other Studies

1 other study(ies) available for nvp-tae684 and Lymphoma--Large-B-Cell--Diffuse

Article	Year
Identification of NVP-TAE684, a potent, selective, and efficacious inhibitor of NPM-ALK. Proceedings of the National Academy of Sciences of the United States of America, 2007, Jan-02, Volume: 104, Issue:1 Constitutive overexpression and activation of NPM-ALK fusion protein [t(2:5)(p23;q35)] is a key oncogenic event that drives the survival and proliferation of anaplastic large-cell lymphomas (ALCLs). We have identified a highly potent and selective small-molecule ALK inhibitor, NVP-TAE684, which blocked the growth of ALCL-derived and ALK-dependent cell lines with IC(50) values between 2 and 10 nM. NVP-TAE684 treatment resulted in a rapid and sustained inhibition of phosphorylation of NPM-ALK and its downstream effectors and subsequent induction of apoptosis and cell cycle arrest. In vivo, NVP-TAE684 suppressed lymphomagenesis in two independent models of ALK-positive ALCL and induced regression of established Karpas-299 lymphomas. NVP-TAE684 also induced down-regulation of CD30 expression, suggesting that CD30 may be used as a biomarker of therapeutic NPM-ALK kinase activity inhibition. Topics: Animals; Apoptosis; Cell Cycle; Cell Line; Humans; Ki-1 Antigen; Lymphoma, Large B-Cell, Diffuse; Mice; Mice, SCID; Phosphorylation; Protein Kinase Inhibitors; Protein-Tyrosine Kinases; Pyrimidines; Signal Transduction; STAT3 Transcription Factor; STAT5 Transcription Factor	2007

Article

Year

Identification of NVP-TAE684, a potent, selective, and efficacious inhibitor of NPM-ALK.

Proceedings of the National Academy of Sciences of the United States of America, 2007, Jan-02, Volume: 104, Issue:1

Constitutive overexpression and activation of NPM-ALK fusion protein [t(2:5)(p23;q35)] is a key oncogenic event that drives the survival and proliferation of anaplastic large-cell lymphomas (ALCLs). We have identified a highly potent and selective small-molecule ALK inhibitor, NVP-TAE684, which blocked the growth of ALCL-derived and ALK-dependent cell lines with IC(50) values between 2 and 10 nM. NVP-TAE684 treatment resulted in a rapid and sustained inhibition of phosphorylation of NPM-ALK and its downstream effectors and subsequent induction of apoptosis and cell cycle arrest. In vivo, NVP-TAE684 suppressed lymphomagenesis in two independent models of ALK-positive ALCL and induced regression of established Karpas-299 lymphomas. NVP-TAE684 also induced down-regulation of CD30 expression, suggesting that CD30 may be used as a biomarker of therapeutic NPM-ALK kinase activity inhibition.

Topics: Animals; Apoptosis; Cell Cycle; Cell Line; Humans; Ki-1 Antigen; Lymphoma, Large B-Cell, Diffuse; Mice; Mice, SCID; Phosphorylation; Protein Kinase Inhibitors; Protein-Tyrosine Kinases; Pyrimidines; Signal Transduction; STAT3 Transcription Factor; STAT5 Transcription Factor

2007