BMS-554417

BMS-554417 potently and selectively inhibits recombinant insulin receptor (IC₅₀ = 50.6 nM), IGF-IR (IC₅₀ = 67.9 nM), and FAK (IC₅₀ = 94.0 nM) kinases in cell-free assays, with ~5-fold selectivity over other tested kinases^[1].
BMS-554417 (72 h) inhibits proliferation of multiple human tumor cell lines in a dose-dependent manner, with IC₅₀ values ranging from 0.146 μM (RD-1) to 2.21 μM (MDA MB 231), and MCF-7 cells (IC₅₀ = 0.22-0.34 μM) are ~18-42-fold more sensitive than OV202 cells (IC₅₀ = 6.5-8.4 μM)^[1].
BMS-554417 (5-20 μM; 1 h) inhibits basal and ligand-induced IGF-IR phosphorylation in MCF-7 and OV202 cells, and insulin-induced insulin receptor phosphorylation in MCF-7 cells, without altering total receptor protein levels^[1].
BMS-554417 (5-20 μM; 1 h) inhibits ligand-induced and basal ERK1/2 and Akt (Ser⁴⁷³) phosphorylation in MCF-7 and OV202 cells, without affecting total ERK1/2, Akt, p38, or JNK protein levels^[1].
BMS-554417, a dual IGF-IR/IR tyrosine kinase inhibitor with balanced potency against both receptors, inhibits the growth of human colon (Colo205), ovarian (OV202), and MCF-7 breast cancer cells in vitro^[2].
BMS-554417 completely inhibits IGF-1R/InsR phosphorylation and increases HER2 phosphorylation (with further enhancement by EGF) in OV202 ovarian cancer cells^[3].
BMS-554417 (72 h) exhibits synergistic antiproliferative activity with the panHER inhibitor BMS-599626 (HY-10251) in OV202 ovarian cancer cells^[3].
BMS-554417 (5 μM; 24 h) abrogates LR3 IGF-I-induced G₁ to S phase progression and nuclear accumulation of cyclin D1 in MCF-7 cells^[1].
BMS-554417 (IC₉₀ concentrations, 2.5-10 μM; 72 h) induces apoptosis in MCF-7, OV202, and Jurkat cells, with apoptosis in Jurkat cells occurring via the mitochondrial pathway (independent of death receptor signaling)^[1].

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