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ENaC inhibitors for the treatment of cystic fibrosis

机译:enac抑制剂治疗囊性纤维化

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摘要

The epithelial Na+ channel, ENaC, is a key regulator of the volume of airway surface liquid in the human airway epithelium. In cystic fibrosis (CF), Na+ hyperabsorption through ENaC in the absence of CFTR-mediated anion secretion results in the dehydration of respiratory secretions and the impairment of mucociliary clearance. The hypothesis of utilizing an ENaC-blocking molecule to facilitate restoration of the airway surface liquid volume sufficiently to allow normal mucociliary clearance is of interest in the management of lung disease in CF patients. This article summarizes the published patent applications from 2010 that claim approaches to inhibit the function of ENaC for utility in the treatment of CF. Patents were located though SciFinder?, using "ENaC" as the keyword from 2010 onwards; documents not relevant to CF were then manually removed.
机译:上皮NA +通道ENAC是人类气道上皮中气道表面液体的关键调节器。 在囊性纤维化(CF)中,通过CFTR介导的阴离子分泌的enac通过ENAC导致呼吸分泌物的脱水以及粘膜间隙的损害。 利用ENAC阻断分子的假设促进气道表面液体体积的恢复以允许正常的粘液间隙对CF患者肺病的管理感兴趣。 本文总结了来自2010年的已发布的专利申请,其中要求抑制ENAC在治疗中抑制ENAC功能的方法。 虽然Scifinder,但使用“ENAC”作为2010年的关键字的专利; 然后手动删除与CF无关的文件。

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