BI-4659 

BI-4659 is a TGFβRI and PDGFRα inhibitor with IC₅₀ values of 19 nM and 99 nM, respectively. BI-4659 inhibits the kinase activities of TGFβRI and PDGFRα, blocks the downstream TGFβRI signaling pathway, and reduces the phosphorylation level of Smad2/3 without altering the expression of TGF-β1. BI-4659 is applicable to research related to pulmonary fibrosis, cancer, and renal ischemia-reperfusion injury^[1][2].

BI-4659 (75 min) inhibits TGFβRI-mediated phosphorylation of Smad2/3 in HaCaT cells with an EC₅₀ of 185 nM^[1].
BI-4659 (up to 1 μM; 24 h) shows no significant cytotoxicity in HaCaT cells at concentrations as high as 1 μM following a 24 h incubation^[1].
BI-4659 (1 μM; 24 h) inhibits the TGF-β-Smad2/3 pathway in mouse bone marrow-derived neutrophils, thereby blocking sFgl2-MSC-induced transformation of neutrophils into an anti-inflammatory N2-like phenotype, inhibition of neutrophil extracellular trap formation, and regulation of inflammatory cytokine secretion^[2].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

440.54

C₂₇H₂₈N₄O₂

894784-05-5

Solid

Off-white to yellow

CN(C)CC(C=C1)=CC=C1N/C(C2=CC=CC=C2)=C3C4=CC=C(C(NCC)=O)C=C4NC/3=O

Room temperature in continental US; may vary elsewhere.

• [1]. Roth GJ, et al. Design, synthesis, and evaluation of indolinones as inhibitors of the transforming growth factor β receptor I (TGFβRI). J Med Chem. 2010;53(20):7287-7295.  [Content Brief]

  [2]. Chen GS, et al. Overexpression of Soluble Fibrinogen-like Protein 2 in MSCs Ameliorates Renal Ischemia-Reperfusion Injury in Mice by Modulating Neutrophils. Balkan Med J. 2026;43(3):136-150.  [Content Brief]