Cat. No. 1614
Chemical Name: 4-[4-(1,3-benzodioxol-5-yl)-5-(2-py
Biological ActivityPotent and selective inhibitor of the transforming growth factor-β (TGF-β) type I receptor activin receptor-like kinase ALK5 (IC50 = 94 nM), and its relatives ALK4 and ALK7. Suppresses TGF-β-induced proliferation of human osteosarcoma cells. Stimulates proliferation, differentiation and sheet formation of ESC-derived endothelial cells. Inhibits TGF-β-induced EMT, migration, invasion and VEGF secretion in several human cancer cell lines.
Licensing InformationSold for research purposes under agreement from GlaxoSmithKline
The technical data provided above is for guidance only. For batch specific data refer to the Certificate of Analysis.
All Tocris products are intended for laboratory research use only.
Certificate of Analysis / Safety Data Sheet
Inman et al (2002) SB-431542 is a potent and specific inhibitor of transforming growth factor-β superfamily type I activin receptor-like kinase (ALK) receptors ALK4, ALK5, and ALK7. Mol.Pharmacol. 62 65. PMID: 12065756.
Laping et al (2002) Inhibition of transforming growth factor (TGF)-β1-induced extracellular matrix with a novel inhibitor of the TGF-β type I receptor kinase activity: SB-431542. Mol.Pharmacol. 62 58. PMID: 12065755.
Matsuyama et al (2003) SB-431542 and Gleevec inhibit transforming growth factor-β-induced proliferation of human osteosarcoma cells. Cancer Res. 63 7791. PMID: 14633705.
Watabe et al (2003) TGF-beta receptor kinase inhibitor enhances growth and integrity of embryonic stem cell-derived endothelial cells. J.Cell Biol. 163 163. PMID: 14676305.
Halder et al (2005) A specific inhibitor of TGF-beta receptor kinase, SB-431542, as a potent antitumor agent for human cancers. Neoplasia 7 509. PMID: 15967103.
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Keywords: SB 431542, supplier, Potent, selective, inhibitors, TGF-βRI, TGF-β, TGF-betaRI, TGFbRI, TGFbR1, tgf-b1, ALK4, ALK7, Transforming, Growth, Factors, Beta, Receptors, Receptor, Serine/Threonine, Kinases, RSTKs, SB431542, stem, cells, GlaxoSmithKline, GSK, EMT, migration, invasion, epithelial, mesenchymal, transition