Inhibitor of mitochondrial pyruvate dehydrogenase kinase (PDK). Shifts pyruvate metabolism from glycolysis and lactate production to glucose oxidation in the mitochondria. Induces mitochondrial-dependent apoptosis and reverses the inhibition/downregulation of KV1.5 channels in cancer but not normal cells. Decreases tumor growth in vitro and in vivo.
|Storage||Desiccate at RT|
The technical data provided above is for guidance only. For batch specific data refer to the Certificate of Analysis.
All Tocris products are intended for laboratory research use only.
|Solvent||Max Conc. mg/mL||Max Conc. mM|
Preparing Stock Solutions
The following data is based on the product molecular weight 150.92. Batch specific molecular weights may vary from batch to batch due to solvent of hydration, which will affect the solvent volumes required to prepare stock solutions.
|Concentration / Solvent Volume / Mass||1 mg||5 mg||10 mg|
|1 mM||6.63 mL||33.13 mL||66.26 mL|
|5 mM||1.33 mL||6.63 mL||13.25 mL|
|10 mM||0.66 mL||3.31 mL||6.63 mL|
|50 mM||0.13 mL||0.66 mL||1.33 mL|
References are publications that support the products' biological activity.
Bowker-kinley et al (1998) Evidence for existence of tissue-specific regulation of the mammalian pyruvate dehydrogenase complex. Biochem.J. 329 191 PMID: 9405293
Bonnet et al (2007) A mitochondria-K+ channel axis is suppressed in cancer and its normalization promotes apoptosis and inhibits cancer growth. Cancer Cell 11 37 PMID: 17222789
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Keywords: DCA, supplier, Mitochondrial, pyruvate, dehydrogenase, kinase, PDK, inhibitors, inhibits, Kinases, Other, Kinases, Other, Kinases, Tocris Bioscience
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