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Description

A cell-permeable binaphthol-sulfonamide that competes against pY proteins for Stat3 SH2 domain binding. Shown to inhibit G-CSF-induced Stat3 tyr705 phosphorylation in human AML cell lines and primary cultures (IC50 from 4.1 to 18 µ,M). Also shown to inhibit G-CSF-stimulated TIE2, MATK, JAK1, and HGFR phosphorylation (by 90%, 50%, 40%, and 40%, respectively, 10 µ,M C188-9), but not 15 other phosphoproteins (<=30% inhibition), including pERK1/2 and pAKT, in Kasumi-1 cells., A cell-permeable binaphthol-sulfonamide that competes against pY proteins for Stat3 SH2 domain binding. Shown to inhibit G-CSF-induced (100 ng/ml for 15 min following 1 h drug pretreatment) Stat3 tyr705 phosphorylation in 6 human AML cell lines (IC50 from 4.1 to 8.3 µ,M) and 4 primary pediatric AML cultures (IC50 from 8 to 18 µ,M). Long-term treatments (24 h for lines and 48 h for primary cultures) result in apoptosis induction (Annexin V-PE staining) in 7 AML lines (EC50 from 8.4 to 43.6 µ,M) and CD34+ populations from 5 primary pediatric AML samples (EC50 from 0.8 to25 µ,M). Selectivity studies using Kasumi-1 cells reveals concomitant inhibitions of G-CSF-stimulated TIE2, MATK, JAK1, and HGFR phosphorylation (by 90%, 50%, 40%, and 40%, respectively, 10 µ,M C188-9), but not 15 other phosphoproteins (<=30% inhibition), including pERK1/2 and pAKT.