Bioactivity | DASA-58 is a potential pyruvate kinase isozyme (PKM2) allosteric activator. DASA-58 can be used for the research of metabolism and kinds of cancer[1]. | ||||||||||||
Invitro | DASA-58 (15 μM; 2 h) potentiates the antitumor effects of other metabolic stressors[1].DASA-58 (15 μM; 24 h, 72 h) enhances pyruvate kinase activity in breast cancer cells without a clear effect on proliferation[1].DASA-58 (30 μM, 60 μM; 0-72 h) enhances extracellular acidification and lactate levels in BCa cell lines and induce extracellular acidification levels in prostate cancer cell lines[1].DASA-58 (15 μM, 30 μM; 0-72 h) affects respiration levels in BCa cells without an indication of mitochondrial damage[1].DASA-58 (15 μM; 0-72 h) not rescues TXNIP levels in any combintion and mitochondrial inhibitors enhance PKM2 effects on activating AMPK signaling (T172 phosphorylation of AMPK) [1].DASA-58 (15 μM; 0-72 h) leads to depletion in TXNIP levels independent of AMPK and ER signaling, and not through enhanced proteasomal degradation but rather depleted upstream glycolytic intermediates[1]. Cell Viability Assay[1] Cell Line: | ||||||||||||
Name | DASA-58 | ||||||||||||
CAS | 1203494-49-8 | ||||||||||||
Formula | C19H23N3O6S2 | ||||||||||||
Molar Mass | 453.53 | ||||||||||||
Appearance | Solid | ||||||||||||
Transport | Room temperature in continental US; may vary elsewhere. | ||||||||||||
Storage |
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Reference | [1]. Fadi Almouhanna, et al. Pharmacological activation of pyruvate kinase M2 reprograms glycolysis leading to TXNIP depletion and AMPK activation in breast cancer cells. Cancer Metab. 2021 Jan 22;9(1):5. |