SLC4A11 mutations cause corneal endothelial dystrophies. This degenerative condition leads to corneal haze, edema, and vision loss. SLC4A11 is a recently identified membrane transporter, of which multiple substrates have been suggested. Intracellular pH measurements in SLC4A11‐expressing PS120 cells revealed that SLC4A11 is NH3/NH4+ and H+ permeable. To further characterize SLC4A11 substrates and transport stoichiometry, we performed patch‐clamp recordings in SLC4A11‐PS120 cells. We found that extracellular 10mM NH3/NH4+ induced inward current, which was inhibited by bath acidification and potentiated by bath alkalinization. Current density (pA/pF) at pHo 6.5, 7.5 and 8.5 were ‐0.22±0.19, ‐6.18±1.09, ‐18.43±3.43, respectively (mean±SE, p<0.001). Reversal potential shift in response to [NH3]o and pHo was consistent with an NH3/H+ coupled transport model. 10mM methylammonium induced smaller current (p<0.05) with similar pH sensitivity. Removal of K+, Na+, Cl‐ did not affect SLC4A11 NH3/H+ transport (K+ p=0.90, Na+ p=0.06, Cl‐ p=0.65), suggesting neither Na+, K+, nor Cl‐ is substrate. Stoichiometry of SLC4A11 NH3:H+ transport was estimated by measuring Erev at different [NH3]o. A plot of Erev against log[NH3]o was linear, and the slope was consistent with a 1:2 stoichiometry. We here identify SLC4A11 as a new member of ammonia channels/transporters, such as AQP8, Rh, MEP, and Amt.Grant Funding Source: Supported by 5R01EY008834(JAB); 5R01HL115140(AGO).