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. 2021 Apr 28;11:9161. doi: 10.1038/s41598-021-88150-6

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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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PLK1 inhibitors induce embryonic lethality and sterility phenotypes in nematodes. (A) PLK1 inhibitors from three core scaffolds including the 2,4-Dianilinopyrimidines (GSK1520489A), the 2,4-Dianilino pyrrolopyrimidines (GSK2220400A) and Benzimidazole N-thiophenes (GSK580432A, GSK479719A, GSK483724A, and GSK448459A) induce phenotypes consistent with loss of C. elegans PLK-1 including sterility (Ste) and embryonic lethality (Emb) resulting in the population growth defects indicated by the colour coded scale (nb, no bacteria remaining in the well). (B) The three Benzimidazole N-thiophene PLK1 inhibitors tested (GSK483724A, GSK479719A and GSK580432A) inhibit C. elegans PLK-1 kinase activity in vitro with IC50 values of 91 nM, 39 nM and 24 nM respectively.