a potent, selective, and efficacious inhibitor of NPM-ALK fusion protein kinase; structure in first source
Also Known As:
Networked: 11 relevant articles (2 outcomes, 0 trials/studies)

Relationship Network

Bio-Agent Context: Research Results


1. Okamoto, Isamu: 2 articles (11/2012 - 04/2011)
2. Takezawa, Ken: 2 articles (11/2012 - 04/2011)
3. Nishio, Kazuto: 2 articles (11/2012 - 04/2011)
4. Nakagawa, Kazuhiko: 2 articles (11/2012 - 04/2011)
5. Jänne, Pasi A: 2 articles (04/2011 - 12/2010)
6. Gray, Nathanael S: 2 articles (12/2010 - 01/2007)
7. Qiang, Jiankun: 1 article (10/2014)
8. Han, Siqi: 1 article (10/2014)
9. Li, Guangchao: 1 article (10/2014)
10. Yang, Lin: 1 article (10/2014)

Related Diseases

1. Neoplasms (Cancer)
2. Neoplasm Metastasis (Metastasis)
3. Lung Neoplasms (Lung Cancer)
10/01/2014 - "Combined TAE684 with PI3K inhibitor synergistically inhibited the proliferation of EML4-ALK-positive cells in vitro and significantly suppressed the growth of H2228 xenografts in vivo, suggesting the potential clinical application of such combinatorial therapy regimens in patients with EML4-ALK positive lung cancer."
11/15/2012 - "We established lines of EML4-ALK-positive H3122 lung cancer cells that are resistant to the ALK inhibitor TAE684 (H3122/TR cells) and investigated their resistance mechanism with the use of immunoblot analysis, ELISA, reverse transcription and real-time PCR analysis, and an annexin V binding assay. "
07/01/2012 - "Endothelial cells and fibroblasts, which produce the EGFR ligands and HGF, respectively, decreased the sensitivity of EML4-ALK lung cancer cells to crizotinib and TAE684, respectively. "
07/01/2012 - "We tested the effects of ligands produced by endothelial cells and fibroblasts, and the cells themselves, on the susceptibility of EML4-ALK lung cancer cell lines to crizotinib and TAE684, a selective ALK inhibitor active against cells with ALK amplification and gatekeeper mutations, both in vitro and in vivo. "
04/15/2011 - "The specific ALK inhibitor TAE684 induced apoptosis that was accompanied both by upregulation of BIM, a proapoptotic member of the Bcl-2 family, and by downregulation of survivin, a member of the inhibitor of apoptosis protein (IAP) family, in EML4-ALK-expressing NIH 3T3 cells as well as in H3122 human lung cancer cells harboring endogenous EML4-ALK. "
4. Neuroblastoma
5. Lymphoma (Lymphomas)

Related Drugs and Biologics

1. Paclitaxel (Taxol)
2. Carboplatin (JM8)
3. Phosphotransferases (Kinase)
4. WHI P154
5. Inhibitor of Apoptosis Proteins
6. Annexin A5
7. Ligands

Related Therapies and Procedures

1. Heterologous Transplantation (Xenotransplantation)