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. 2017 Jul 6;6(4):188–200. doi: 10.5527/wjn.v6.i4.188

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©The Author(s) 2017. Published by Baishideng Publishing Group Inc. All rights reserved.

Open-Access: This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/

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Tesevatinib treatment in the PCK model of autosomal recessive polycystic kidney disease. Compared to wild-type SD control kidneys (A) at PN90, PCK cystic kidneys (C) are significantly enlarged by PN90. TSV treatment results in a dose-dependent reduction in the overall kidney size at doses of 7.5 mg/kg per day (D) and 15 mg/kg per day (E) when compared to untreated PCK cystic kidneys at PN90 (C). Treatment of wildtype SD with 15 mg/kg per day did not result in significant reduction of overall kidney size (B) compared to untreated wildtype SD animals. This correlates directly with the total kidney weight (TKW) of each group listed in Table 2 (Treatment interval: PN30-PN90). TSV: Tesevatinib.