Eact

Eact is an activator of the calcium-activated chloride channel anoctamin 1 (ANO1).¹ It increases chloride currents in FRT cells expressing human ANO1 (EC₅₀ = 3 µM). It is selective for ANO1 over cystic fibrosis transmembrane conductance regulator (CFTR) chloride channels and epithelial sodium channels (ENaCs) in FRT cells at 10 µM. Eact (20 µM) increases the rate of submucosal gland fluid secretion in human bronchi isolated from patients with cystic fibrosis and healthy individuals. It increases production of mitochondrial reactive oxygen species (ROS), reduces the mitochondrial membrane potential, and induces apoptosis in rat lung microvascular endothelial cells (RLMVECs), as well as reduces total cell counts in pulmonary artery endothelial cell populations isolated from patients with idiopathic pulmonary arterial hypertension (IPAH).² Eact also activates transient receptor potential vanilloid 1 (TRPV1) in HEK293T cells expressing the mouse receptor (EC₅₀ = 11.6 µM) and induces scratching and licking behaviors in wild-type, but not Trpv1^-/-, mice.³

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1. Namkung, W., Yao, Z., Finkbeiner, W.E., et al. Small-molecule activators of TMEM16A, a calcium-activated chloride channel, stimulate epithelial chloride secretion and intestinal contraction. The FASEB Journal 25(11), 4048-4062 (2011).

2. Allawzi, A.M., Vang, A., Clements, R.T., et al. Activation of anoctamin-1 limits pulmonary endothelial cell proliferation via p38-mitogen-activated protein kinase-dependent apoptosis. Am. J. Respir. Cell Mol. Biol. 58(5), 658-667 (2018).

3. Liu, S., Feng, J., Luo, J., et al. Eact, a small molecule activator of TMEM16A, activates TRPV1 and elicits pain- and itch-related behaviours. Br. J. Pharmacol. 173(7), 1208-1218 (2016).