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Sigma Aldrich Fine Chemicals Biosciences Lactate Dehydrogenase Inhi

Catalog No. 502900263
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A cell-permeable quinolinesulfonamide compound that acts as potent and reversible inhibitor of lactate dehydrogenase A (IC50 2.6 nM for human LDH-A). The inhibition appears to be competitive with respect to NADH and non-competitive with respect to pyruvate. Exhibits high selectivity over LDH-B (IC50 43 nM) and does not affect the activity of 32 other enzymes receptors and ion-channels even at high concentration (~ 10 181M). Rapidly reduces lactate production in hepatocellular (EC50 400 and 588 nM in Snu398 and HepG2 cells respectively) and breast carcinoma cell lines and induces PKM2 activation (EC50 600 nM in Snu398 cells). Shown to increase mitochondrial oxygen consumption rate (EC50 500 and 900 nM in Snu398 and HepG2 cells respectively) and causes a diminution in extracellular acidification rates (EC50 600 nM in both cell lines). Shown to downregulate the ability of A549 cells to form tumorspheres and diminishes the number of CD24/CD44-positive cells in HMLER system and i

Catalog No. 50-290-0263 Supplier Sigma Aldrich Fine Chemicals Biosciences Supplier No. 5336600001
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A cell-permeable quinolinesulfonamide compound that acts as potent and reversible inhibitor of lactate dehydrogenase A (IC50 2.6 nM for human LDH-A). The inhibition appears to be competitive with respect to NADH and non-competitive with respect to pyruvate. Exhibits high selectivity over LDH-B (IC50 43 nM) and does not affect the activity of 32 other enzymes receptors and ion-channels even at high concentration (~ 10 181M). Rapidly reduces lactate production in hepatocellular (EC50 400 and 588 nM in Snu398 and HepG2 cells respectively) and breast carcinoma cell lines and induces PKM2 activation (EC50 600 nM in Snu398 cells). Shown to increase mitochondrial oxygen consumption rate (EC50 500 and 900 nM in Snu398 and HepG2 cells respectively) and causes a diminution in extracellular acidification rates (EC50 600 nM in both cell lines). Shown to downregulate the ability of A549 cells to form tumorspheres and diminishes the number of CD24/CD44-positive cells in HMLER system and i

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