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Objectives Previous findings in mice revealed that SLC26A9, a recently identified epithelial chloride channel, is essential for preventing airway obstruction associated with IL13-induced airway inflammation. These results suggest that SLC26A9 may be a promising alternative Cl − channel in mucoobstructive lung diseases [e.g. cystic fibrosis (CF)]. Thus, we functionally characterized a newly generated epithelial cell line with stable expression of SLC26A9 to investigate molecular regulation. Methods Fisher rat thyroid (FRT) cells were stably transduced with a HA-tagged SLC26A9 construct. Transepithelial Cl − currents were measured by applying a Cl − gradient in Ussing chambers. Whole-cell patch clamp experiments were performed. Results SLC26A9 expression in transduced FRT (FRT-SLC) cells was found at high levels. Transepithelial measurements revealed that the basal short circuit current (I sc ) was significantly increased in FRT-SLC (12.3±2.0 µA/cm 2 P 2 ) cell monolayers. CAMP (IBMX/forskolin)-stimulated Cl − secretion was significantly increased in FRT-SLC compared to FRT-CTL cells (ΔI sc = 4.9±0.5 vs. ΔI sc = 0.7±0.2 µA/cm 2 P − current in FRT-SLC cells and a similar inhibitor selectivity. Conclusion In FRT-SLC cells, SLC26A9 contributes to constitutive and cAMP-stimulated Cl − currents. This established epithelial cell model overexpressing SLC26A9 may be useful for further studies of the regulation and pharmacological activation of SLC26A9 as an alternative Cl − channel in CF.