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. 2021 Jan 22;9:5. doi: 10.1186/s40170-021-00239-8

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© The Author(s) 2021

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/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

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Fig. 6 — PKM2 activation potentiates the antitumor effects of other metabolic stressors. a, b Total protein staining using SRB assay (a) or metabolically active cells using MTT assay (b) showing the efficacy of combining DASA-58 (15 μM) with different metabolic stressors/inhibitors of glycolytic branching pathways in BCa cells. Data are presented as % survival normalized to the mock treatment and daggers (†) used to indicate statistical significance between the single and the combo treatment. c Schematic illustration representing the hypothesis of combining the PKM2 activator with other metabolic modulating drugs (red font)