Bio-Connect
Chemical Structure
Chemical Structure
Chemical Structure

Sodium dichloroacetate [DCA] [2156-56-1]

Research Use Only
AG-CR1-3684
AdipoGen Life Sciences
Estimated Purity>98%
Product group Chemicals
Molecular Weight127.9 . 23.0
Price on request
Packing Size
Large volume orders?
Order with a bulk request

Overview

  • Supplier
    AdipoGen Life Sciences
  • Product Name
    Sodium dichloroacetate [DCA] [2156-56-1]
  • Delivery Days Customer
    10
  • Certification
    Research Use Only
  • Estimated Purity
    >98%
  • Hazard Information
    Non-hazardous,Warning
  • Molecular Formula
    C2HCl2O2 . Na
  • Molecular Weight
    127.9 . 23.0
  • Scientific Description
    Chemical. CAS: 2156-56-1. Formula: C2HCl2O2 . Na. MW: 127.9 . 23.0. Synthetic. Analog of acetic acid. Mitochondrial pyruvate dehydrogenase kinase (PDK) inhibitor, consequently activating pyruvate dehydrogenase (PDH). Decreases glycolysis. Shifts pyruvate metabolism from glycolysis and lactate production to glucose oxidation in the mitochondria. Antitumor agent. Decreases tumor growth in vitro and in vivo. Induces mitochondrial-dependent apoptosis. Useful agent for immunometabolism research. Glucose entering the cell is metabolized by glycolysis to pyruvate. Most of the pyruvate in non-cancerous cells enters the mitochondria under aerobic conditions and a small fraction is metabolized to lactate. PDH in mitochondria converts pyruvate into acetyl-CoA, which enters the TCA cycle. In cancer cells, the oxidative (mitochondrial) pathway of glucose utilization is suppressed and most of the pyruvate is converted into lactate (Warburg effect). The relative activities of LDH and PDH therefore determine the fate of pyruvate. PDK inhibits PDH through phosphorylation and regulates its activities, resulting in suppression of the TCA cycle and mitochondrial respiration. This renders PDK a promising target for the treatment of various cancers. - Mitochondrial pyruvate dehydrogenase kinase (PDK) inhibitor, consequently activating pyruvate dehydrogenase (PDH). Decreases glycolysis. Shifts pyruvate metabolism from glycolysis and lactate production to glucose oxidation in the mitochondria. Antitumor agent. Decreases tumor growth in vitro and in vivo. Induces mitochondrial-dependent apoptosis. Useful agent for immunometabolism research. Glucose entering the cell is metabolized by glycolysis to pyruvate. Most of the pyruvate in non-cancerous cells enters the mitochondria under aerobic conditions and a small fraction is metabolized to lactate. PDH in mitochondria converts pyruvate into acetyl-CoA, which enters the TCA cycle. In cancer cells, the oxidative (mitochondrial) pathway of glucose utilization is suppressed and most of the pyruvate is converted into lactate (Warburg effect). The relative activities of LDH and PDH therefore determine the fate of pyruvate. PDK inhibits PDH through phosphorylation and regulates its activities, resulting in suppression of the TCA cycle and mitochondrial respiration. This renders PDK a promising target for the treatment of various cancers.
  • SMILES
    ClC(Cl)C([O-])=O.[Na+]
  • Storage Instruction
    2°C to 8°C,-20°C
  • UNSPSC
    12352200

References

  • Activation of pyruvate dehydrogenase in perfused rat heart by dichloroacetate: S. Whitehouse & P.J. Randle; Biochem. J. 134, 651 (1973)
  • The pharmacology of dichloroacetate: P.W. Stacpoole; Metabolism 38, 1124 (1989)
  • A mitochondria-K+ channel axis is suppressed in cancer and its normalization promotes apoptosis and inhibits cancer growth: S. Bonnet, et al.; Cancer Cell 11, 37 (2007)
  • Distinct Structural Mechanisms for Inhibition of Pyruvate Dehydrogenase Kinase Isoforms by AZD7545, Dichloroacetate, and Radicicol: M. Kato, et al.; Cell Structure 15, 992 (2007)
  • Metabolic Modulation of Glioblastoma with Dichloroacetate: E.D. Michelakis, et al.; Sci. Transl. Med. 2, 31 (2010)
  • PDK1 inhibition is a novel therapeutic target in multiple myeloma: S. Fujiwara, et al.; Br. J. Cancer 108, 170 (2013)1
  • A guide to immunometabolism for immunologists: L.A. O'Neill, et al.; Nat. Rev. Immunol. 16, 553 (2016)
  • The pyruvate dehydrogenase complex in cancer: An old metabolic gatekeeper regulated by new pathways and pharmacological agents: E. Saunier, et al.; Int. J. Cancer 138, 809 (2016) (Review)
  • The PDK1 Inhibitor Dichloroacetate Controls Cholesterol Homeostasis Through the ERK5/MEF2 Pathway: A.U. Haq Khan, et al.; Nat. Sci. Rep. 7, 10654 (2017)
  • Dichloroacetate induces regulatory T-cell differentiation and suppresses Th17-cell differentiation by pyruvate dehydrogenase kinase-independent mechanism: N. Makita, et al.; J. Pharm. Pharmacol. 69, 43 (2017)