Search term Biochemical Reagent has been found in the following products: 35

Biochemical Reagent

SB 431542, >98%, BC261

  • CAS No : 301836-41-9
  • Formula : C22H16N4O3
  • MW : 384.39
  • Purity : > 98%
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Cat No Size Price
BC261-005 5 mg $ 135.00 Add to cart
BC261-010 10 mg $ 195.00 Add to cart
BC261-050 50 mg $ 650.00 Add to cart
IC50 94 nM
Targets ALK5
Solubility 76 mg/mL in DMSO
3 mg/mL in Ethanol
SB 431542 is a potent and selective inhibitor of ALK5 with IC50 of 94 nM, 100 -fold more selective for ALK5 than p38 MAPK and other kinases. SB 431542 inhibits the activin type I receptor ALK4 and the nodal type I receptor ALK7, which are responsible for the phosphorylation of Smad2. SB 431542 has little effect on ALK1, ALK2, ALK3, and ALK6, which show phosphorylation of Smad1. SB 431542 is a selective inhibitor of endogenous activin but has no apparent effect on BMP signaling. SB431542 could induce both Smad2/Smad4- and Smad3/Smad4 -dependent transcription. In A498 cells, SB 431542 inhibits production of TGF β1-induced collagen lα1 and PAI-1 mRNA with IC50 of 60nM and 50nM, respec -tively. Inaddition, SB431542 inhibits production of TGF-β-1 induced fibronectin mRNA and protein with IC50 and 62nM and 22nM, respectively. SB 431542 blocks the TGF-β-mediated growth factors, including PDGF-A, FGF-2 and HB-EGF, leading to an increase in proliferation of MG63 cells. SB 431542 also inhibits TGF -β-induced c-Myc and p21 WAF1/CIP1. 

SB 431542 significantly supresses TGF-β-induced G1 arrest, leading to accumulation of cells in the S phase of the cell cycle in FET, RIE, and Mv1Lu cells. SB 431542 also inhibits TGF-β-induced epithelial to mesemchymal transition (EMT) in NMuMG and PANC-1 cells. SB 431542 significantly elevates the expression of CD86 in BM-DCs and that of CD83 within CD11c+ cells supressed by TGF-β. SB 431542 is able to induce NK activity through functional maturation and IL-12 production of human DCs. SB 431542 triggers cytotoxic T lymphocyte (CTL) activities in the colon-26 carci -noma models and is most likely to produce antitumor immunological outcomes through alteration of DC function supressed by TCF-β.