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. 2023 Mar 13;199(1):13–23. doi: 10.1007/s10549-023-06895-2

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© The Author(s) 2023

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. 1 — On target off-tumor activity comparison among different PI3K inhibitors: taselisib showed similar cytotoxicity on both B cells and T47D breast cancer cell (PIK3CA H1047R), while MEN1611 was significantly less toxic on B cells focusing to an intra-drug analysis. The same was for alpelisib, which showed higher activity on breast cancer cells compared to B cells. Idelalisib, as expected, demonstrated poor activity on breast cancer setting and high activity on B cells (a, b) Inhibition of pAKT in a PI3K delta-driven model (immortalized B-cells) after 2 h of drug exposure. Capillary immunoassay analysis of phospho and total AKT following treatment with MEN1611 and other PI3Ki. Representative lane view image of phospho an total AKT protein levels (A). Means ± SD of pAKT protein levels normalized to total AKT and expressed as percentage of DMSO-treated samples (N = 3) (c, d)