产品
编 号：F069085
分子式：C19H23N3O6S2
分子量：453.53
分子式：C19H23N3O6S2
分子量：453.53
产品类型
规格
价格
是否有货
10mM*1mL in DMSO
924
In-stock
1mg
396
In-stock
5mg
840
In-stock
10mg
1520
In-stock
50mg
5040
In-stock
结构图
CAS No: 1203494-49-8
产品详情
生物活性：
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.
体外研究：
DASA-58 (15 μM; 2 h) potentiates the antitumor effects of other metabolic stressors.?DASA-58 (15 μM; 24 h, 72 h) enhances pyruvate kinase activity in breast cancer cells without a clear effect on proliferation.?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.?DASA-58 (15 μM, 30 μM; 0-72 h) affects respiration levels in BCa cells without an indication of mitochondrial damage.?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) .?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.
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.
体外研究：
DASA-58 (15 μM; 2 h) potentiates the antitumor effects of other metabolic stressors.?DASA-58 (15 μM; 24 h, 72 h) enhances pyruvate kinase activity in breast cancer cells without a clear effect on proliferation.?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.?DASA-58 (15 μM, 30 μM; 0-72 h) affects respiration levels in BCa cells without an indication of mitochondrial damage.?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) .?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.
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