Sodium dichloroacetate

SKU: orb1304008

Description

Sodium dichloroacetate (DCA) is a small molecule PDK inhibitor that shifts tumor cell metabolism from glycolysis to oxidative phosphorylation. This action reduces lactate, elevates ROS, and induces apoptosis, making it a valuable tool for studying cancer metabolism in both in vitro and in vivo experimental models.

Research Area

Cell Biology, Immunology & Inflammation, Metabolism Research, Pharmacology & Drug Discovery, Signal Transduction

Key Properties

• CAS Number: 2156-56-1
• MW: 150.92
• Purity: 99.87% (May vary between batches)
• Formula: C₂HCl₂NaO₂
• SMILES: C(C(=O)[O-])(Cl)Cl.[Na+]
• Target: Na-K-Cl cotransporter,Apoptosis,Reactive Oxygen Species,Dehydrogenase,ROS,PDK
• Solubility: H2O:166.66 mg/mL (1104.29 mM);DMSO:26 mg/mL (172.28 mM)

Bioactivity

• Target IC50:
  PDK2:183 μM|L02 cells:21.7 mM|4T1 cells:> 100 μM|MCF-7 cells:12.35 mM|SH-SY5Y cells:17.4 mM|KB cells:1424 μM|A549 cells:20.1 mM|NCI-H1650 cells:16.3 mM|PDK4:80 μM|PC3 cells:15.7 mM|NCI-H4 cells:3892 μM|A375 cells:20.1 mM|Bel-7402 cells:860 μM|HCT116 cells:9.8 mM|BGC-823 cells:1051 μM
• In Vivo:
  METHODS: To study the effect on energy expenditure in ApoE-/- mice, Sodium dichloroacetate (100-150 mg/kg) was administered by gavage once daily for four weeks to ApoE-/- mice fed the western diet model of atherosclerosis. RESULTS: Western diet-fed ApoE-/- mice developed atherosclerotic plaques and hyperlipidemia, as well as obesity, which were significantly ameliorated by the administration of Sodium dichloroacetate. Enhanced glucose oxidation by Sodium dichloroacetate protects against atherosclerosis by inducing hepatic FGF21 expression and BAT activation, thereby increasing the risk of atherosclerosis. atherosclerosis, thereby increasing energy expenditure for calorie production.
• In Vitro:
  METHODS: Tumor cells A549, MO59K and MCF-7 and normal cells SAEC were treated with Sodium dichloroacetate (0.5 mM) for 48 h. Mitochondrial membrane potential ΔΨm was detected using fluorescent dye. RESULTS: Incubation of all three types of tumor cells with Sodium dichloroacetate reversed hyperpolarization and restored ΔΨm to the level of normal cells. In contrast, Sodium dichloroacetate did not alter ΔΨm in SAEC. METHODS: OSCC cell lines HSC-2, HSC-3 and PE15 were treated with Sodium dichloroacetate (1-10 mM) for 24 h. Cell viability was measured using the MST assay. RESULTS: HSC-2 and HSC-3 showed more significant unique sensitivity to the drugs. Compared with HEK 293, the viability of both HSC-2 and HSC-3 was about 30% at 10 mM Sodium dichloroacetate, while the viability of PE15 was 75-80%.

Storage & Handling

• Storage: Powder: -20°C for 3 years | In solvent: -80°C for 1 year | Shipping with blue ice/Shipping at ambient temperature.
• Expiration Date: 12 months from date of receipt.
• Disclaimer: For research use only

Alternative Names

ReactiveOxygenSpecies, Reactive Oxygen Species, Sodium Dichloroacetate, Sodium bichloroacetic acid, Sodium dichloroacetate, Sodium dichloroacetate (DCA), dehydrogenase, DCA sodium salt, DCA, BCA, bichloroacetic acid, Apoptosis, NKCC, PDK, PDH kinase, PDH, PDHK, pyruvate, Pyruvate dehydrogenase kinase, mitochondria, lactic

Compound Identifiers

PubChem CID

517326