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. 2020 Nov 24;124(4):728–735. doi: 10.1038/s41416-020-01151-6

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© The Author(s) 2020

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 license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license 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 license, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 3 — In a typical time-course profiles of PK (grey circles) and DNA-PK inhibition (black squares) after peposertib treatment from one patient treated with peposertib 100 mg QD. DNA-PK inhibition on treatment is expressed as percentage change of p-DNA-PK/t-DNA-PK from the pre-treatment value (time h = 0). In b concentration-dependent inhibition of DNA-PK in response to peposertib treatment. Experimental concentration−response data are shown (open circles) and the line represents the E_max model fit to the data. Bleo bleomycin, DNA-PK DNA-dependent protein kinase, E_max maximum response, p-DNA-PK autophosphorylated form of DNA-PK on Ser²⁰⁵⁶, PK pharmacokinetics, QD once daily, t-DNA-PK total DNA-PK.