ANO1 and cystic fibrosis: 2009). This raises the important question as to whether the CCE-induced rise in [Ca2+]i could translate into TMEM16A stimulation in the ICC that would be beneficial in the treatment of CF patients such as constipation and dysmotility. We observed that CCE accelerated intestinal transit by 53% in the loperamide-treated constipation mouse model compared to loperamide alone (Figure 4(C)). Our results further showed that the bio-active material activated intestinal smooth muscle contraction in isolated mouse colon as shown in Figure 4(B).