YS-01

YS-01 potently inhibits pendrin-mediated Cl⁻/SCN⁻ exchange activity in pendrin-transfected human alveolar epithelial cells, with an IC₅₀ of 4.7 μM; it significantly inhibits LPS-induced increase in apical SCN⁻ concentration in human nasal epithelial cells^[1].
YS-01 (0-100 μM; 10 minutes at 37°C) potently and selectively inhibits human and mouse pendrin-mediated anion exchange across multiple anion pairs in CHO-K1 cells, and shows no activity against a variety of related ion channels and transporters at relevant concentrations^[3].
YS-01 (0-100 μM) inhibits IL-4-induced pendrin-mediated Cl⁻/HCO₃⁻ exchange activity in primary human nasal epithelial cells in a dose-dependent manner, with significant inhibition observed at concentrations as low as 3 μM^[3].
YS-01 (30 μM; 24-48 h) reduces the functional expression of IL-4-induced pendrin protein levels in primary human nasal epithelial cells (without affecting mRNA levels) and exerts no effect on related ion channels^[3].
YS-01 (30 μM; 30 min) inhibits IL-4-induced transepithelial SCN⁻ transport in primary human nasal epithelial cells cultured at an air-liquid interface^[3].
YS-01 reduces IL-4-induced MUC5AC expression and IL-4/IL-13-induced goblet cell hyperplasia in primary human nasal epithelial cells; it rescues the reduction of airway surface liquid volume induced by IL-4 and IL-13 in primary human nasal epithelial cells expressing wild-type pendrin^[3].
YS-01 inhibits IL-4-induced activation of NF-κB in primary human nasal epithelial cells^[3].

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