Phenamil is an inhibitor of transient receptor potential polycystin-L (TRPP3; IC50 = 140 nM) and a derivative of amiloride.[1] It also inhibits the epithelial sodium channel (ENaC; IC50 = 400 nM).[2] Phenamil decreases basal short-circuit currents in human and ovine bronchial epithelial cells with IC50 values of 75 and 116 nM, respectively.[3] It inhibits potassium chloride-induced contractions in isolated rat endothelium-denuded aortic rings (EC50 = 6.76 μM) and increases contractile force in isolated rat right ventricular papillary muscles (EC50 = 16.98 μM).[4] Phenamil (15 and 30 mg/kg per day) reduces pulmonary artery medial wall thickness and decreases right ventricular peak pressure in a rat model of chronic hypoxia-induced pulmonary hypertension.[5]

Reference:
[1]. Dai, X.Q., Ramji, A., Liu, Y., et al. Inhibition of TRPP3 channel by amiloride and analogs. Mol. Pharmacol. 72(6), 1576-1585 (2007).
[2]. Hirsh, A.J., Molino, B.F., Zhang, J., et al. Design, synthesis, and structure - activity relationships of novel 2-substituted pyrazinoylguanidine epithelial sodium channel blockers: Drugs for cystic fibrosis and chronic bronchitis. J. Med. Chem. 49(14), 4098-4115 (2006).
[3]. Hirsh, S.J., Sabater, J.R., Zamurs, A., et al. Evaluation of second generation amiloride analogs as therapy for cystic fibrosis lung disease. J. Pharmacol. Exp. Ther. 311(3), 929-938 (2004).
[4]. Brown, L., Cragoe, E.J., Jr., Abel, K.C., et al. Amiloride analogues induce responses in isolated rat cardiovascular tissues by inhibition of Na+/Ca2+ exchange. Naunyn Schmiedebergs Arch Pharmacol. 344(2), 220-224 (1991).
[5]. Chan, M.C., Weisman, A.S., Kang, H., et al. The amiloride derivative phenamil attenuates pulmonary vascular remodeling by activating NFAT and the bone morphogenetic protein signaling pathway. Mol. Cell. Biol. 31(3), 517-530 (2011).