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. 2021 Mar 18;11:6317. doi: 10.1038/s41598-021-85613-8

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© The Author(s) 2021

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/.

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Dual mechanism of karonudib leads to apoptosis in lymphoma cells. Karonudib was developed to target the nucleotide metabolism by inhibiting the nucleotide pool sanitizing enzyme, MTH1. MTH1 converts oxidized nucleotide triphosphates created by reactive oxygen species (ROS) to the corresponding monophosphate forms, preventing incorporation of oxidized nucleotides into DNA. High ROS levels in lymphoma corresponds to high MTH1 levels. Karonudib inhibits the function of MTH1 and results in increased oxidized nucleotides in the DNA, and the drug also perturbs microtubule polymerization and leads to cell cycle arrest and apoptosis.