產品名稱 SB 505124
產品貨號 Axon 2197 CAS [694433-59-5] MF C20H21N3O2MW 335.40 Purity: 100% Soluble in 0.1N HCl(aq) and DMSO Description Selective inhibitor of TGF-β type I receptors ALK4 and ALK5 (IC50 values 129 nM and 47 nM, respectively). SB 505124 also inhibits the closely related ALK7 receptor, but not the BMP activated receptors (ALK1, 2, 3, and 6). It inhibits downstream TGF-β and Activin induced signaling of Smad2, but not BMP induced signaling of Smad1, -5, or -8. Pretreatment of the cells with SB-505124 blocked TGFβ–induced cell death but had no effect on TNFα–induced toxicity. Additionally, SB-505124 blocks activation of TGFβ induced MAPK pathways but is ineffective when these pathways are induced by EGF. References Certificates Categories Extra info S. DaCosta Byfield et al. SB-505124 is a selective inhibitor of transforming growth factor-beta type I receptors ALK4, ALK5, and ALK7. Mol. Pharmacol. 2004, 65, 744-52.? Certificate of Analysis Material Safety Data Sheet Apoptosis Cell Signaling & Oncology Stem Cell TGF-β RSTK class I; EC 2.7.11.30 TGF-βR Selective inhibitor of TGF-β type I receptors ALK4 and ALK5 Chemical name 2-(4-(benzo[d][1,3]dioxol-5-yl)-2-tert-butyl-1H-imidazol-5-yl)-6-methylpyridine Parent CAS No. [694433-59-5] Order Size Unit Price Stock 5 mg €95.00 In Stock
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SB 505124

Based on 16 reference(s) in Google Scholar 9 10 16

Axon 2197

CAS [694433-59-5]

MF C20H21N3O2
MW 335.40

  • Purity: 100%
  • Soluble in 0.1N HCl(aq) and DMSO

SB 505124

Description

Selective inhibitor of TGF-β type I receptors ALK4 and ALK5 (IC50 values 129 nM and 47 nM, respectively). SB 505124 also inhibits the closely related ALK7 receptor, but not the BMP activated receptors (ALK1, 2, 3, and 6). It inhibits downstream TGF-β and Activin induced signaling of Smad2, but not BMP induced signaling of Smad1, -5, or -8. Pretreatment of the cells with SB-505124 blocked TGFβ–induced cell death but had no effect on TNFα–induced toxicity. Additionally, SB-505124 blocks activation of TGFβ induced MAPK pathways but is ineffective when these pathways are induced by EGF.
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