CNBDA

CNBDA (61 nM - 4 mM; 10 min) potently inhibits the PTPase activity of purified SHP2 with an IC₅₀ of 5 μM, showing 25-fold greater selectivity over the homologous SHP1 enzyme^[1].
CNBDA (200 nM; overnight serum starvation, followed by 10 min EGF stimulation) inhibits the PTPase activity of endogenous SHP2 in BT474 and JIMT-1 HER2-positive breast cancer cells, as evidenced by accumulation of phosphorylated Tyr542-SHP2 following EGF stimulation^[1].
CNBDA (0.25-1 μM; 24-72 h) suppresses proliferation and induces cell death in BT474 and JIMT-1 HER2-positive breast cancer cells with IC₅₀ values of 300 nM and 400 nM, respectively, while nontransformed MCF-10A breast epithelial cells show high resistance to the compound^[1].
CNBDA (0.25-1 μM; 10 days) suppresses anchorage-independent growth of BT474 and JIMT-1 HER2-positive breast cancer cells in a concentration-dependent manner, eliminating colony formation at 1 μM^[1].
CNBDA (200 nM; overnight serum starvation, followed by 10 min to 4 h EGF stimulation) suppresses sustained EGF-induced activation of the Akt and ERK1/2 signaling pathways and downregulates HER2 expression in BT474 and JIMT-1 HER2-positive breast cancer cells^[1].

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