articleNew England Journal of MedicineMar 15, 2023Closed access

Inaxaplin for Proteinuric Kidney Disease in Persons with Two APOL1 Variants

Beth Israel Deaconess Medical Center · Georgetown University · +12 more institutions

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Abstract

Persons with toxic gain-of-function variants in the gene encoding apolipoprotein L1 (APOL1) are at greater risk for the development of rapidly progressive, proteinuric nephropathy. Despite the known genetic cause, therapies targeting proteinuric kidney disease in persons with two APOL1 variants (G1 or G2) are lacking. Download a PDF of the Research Summary. We used tetracycline-inducible APOL1 human embryonic kidney (HEK293) cells to assess the ability of a small-molecule compound, inaxaplin, to inhibit APOL1 channel function. An APOL1 G2–homologous transgenic mouse model of proteinuric kidney disease was used to assess inaxaplin treatment for proteinuria. We then conducted a single-group, open-label, phase 2a…

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