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. 2022 May 26;49(11):3668–3678. doi: 10.1007/s00259-022-05835-4

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© The Author(s) 2022

Open AccessThis 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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Fig. 4 — A Biodistribution in selected tissues in PSN1 tumour-bearing mice 2 h after intravenous injection of [¹⁸F]rucaparib (0.87–2.47 MBq, A_m = 5.5 GBq/μmol) (n=3/group), with or without an excess of unlabelled olaparib or rucaparib (0.5 mg). B Autoradiography of PSN1 tumour sections showing ¹⁸F localisation and the PARP1 occupancy by unlabelled PARP inhibitors (olaparib and rucaparib, red arrows), and immunohistochemical staining of PSN1 tumour sections showing PARP1, 2 and 3 expression. Asterisks indicate levels of significance: *, P < 0.05; **, P < 0.01