Name | sodium dichloroacetate |
Synonyms | SDA erlcyiuanna dichloroctansodny NATRIUMDICHLORACETAT Sodiumdichloracetate SODIUM DICHLOROACETATE sodium dichloroacetate dichloroacetate,sodiumsalt dichloro-aceticacisodiumsalt |
CAS | 2156-56-1 |
EINECS | 218-461-3 |
InChI | InChI=1/C2H2Cl2O2.Na/c3-1(4)2(5)6;/h1H,(H,5,6);/q;+1/p-1 |
InChIKey | LUPNKHXLFSSUGS-UHFFFAOYSA-M |
Molecular Formula | C2HCl2NaO2 |
Molar Mass | 150.92 |
Melting Point | 198 °C (dec.) (lit.) |
Boling Point | 194°C at 760 mmHg |
Flash Point | 75.6°C |
Water Solubility | soluble in cold water |
Solubility | soluble in cold water |
Vapor Presure | 0.196mmHg at 25°C |
Appearance | White powder |
Color | White |
PH | 6.0 to 8.5(50g/L, 25 ℃) |
Storage Condition | Inert atmosphere,2-8°C |
Stability | Hygroscopic |
Sensitive | Moisture Sensitive |
MDL | MFCD00070489 |
Physical and Chemical Properties | Appearance: White Crystal Melting Point: 189-192°C |
In vitro study | DCA can cause apoptosis in human lung, breast and brain cancer cells. After DCA treatment, the ROS level in cancer cells increased, MMP depolarization, and apoptosis could be increased in vivo and in vitro. DCA inhibits pyruvate dehydrogenase kinase (PDK) activity and thus stimulates mitochondrial pyruvate dehydrogenase (PDH). When PDH is off, PDH no longer converts pyruvate to acetyl-CoA (required for mitochondrial respiration and glucose-dependent oxidative phosphorylation processes). Thus, DCA converts cell metabolism from glycolysis to glucose oxidation, reduces mitochondrial membrane potential, and promotes the opening of mitochondrial transport pores. This series of metabolic transitions contributes to the translocation of pro-apoptotic mediators such as cyt c and AIF. Thus, DCA can drive cancer cell suicide through an apoptotic response. |
In vivo study | DCA acts as a cytostatic agent in vitro and in vivo without causing programmed cell death (apoptosis). DCA is a safe drug with no cardiac, pulmonary, renal or bone marrow toxicity. The most serious side effects include peripheral neuropathy, a reversible process. DCA has anti-cancer activity in several cancer types, including colon cancer, prostate cancer, ovarian cancer, neuroblastoma, lung cancer, cervical cancer, endometrial, cholangiocarcinoma, sarcoma, and T-cell lymphoma. Some other anti-tumor effects of DCA have also been reported, including blocking angiogenesis, changing the expression of HIF-1α, changing the V-ATPase of pH regulator and MCT1, other cell survival regulators such as PUMA, GLUT1, changes in Bcl2 and p53. In a rat model of highly metastatic breast cancer, DCA significantly reduced the metastatic burden in the lung. In Vivo administration of DCA-Na induced a 20% improvement in survival and reduced tumor diameter, volume and weight without affecting body weight and avoiding metastasis in C57BL/6 mice. |
Risk Codes | R36/37/38 - Irritating to eyes, respiratory system and skin. R40 - Limited evidence of a carcinogenic effect |
Safety Description | S26 - In case of contact with eyes, rinse immediately with plenty of water and seek medical advice. S37/39 - Wear suitable gloves and eye/face protection S36 - Wear suitable protective clothing. S36/37 - Wear suitable protective clothing and gloves. |
UN IDs | 2811 |
WGK Germany | 2 |
RTECS | AG9275000 |
HS Code | 29154000 |
EPA chemical information | Information provided by: ofmpub.epa.gov (external link) |
biological activity | Sodium dichloroacetate (DCA, Dichloroacetic acid, bichloroacetic acid, BCA) is a specific inhibitor of pyruvate dehydrogenase kinase (PDK), and its IC50 values for PDK2 and PDK4 are 183 and 80 μM respectively. It can inhibit Na -K -2Cl- cotransporter and mitochondrial potassium channel axis. Sodium dichloroacetate can increase the production of reactive oxygen species, cause apoptosis of cancer cells, and inhibit tumor growth. |
Target | Value |
PDK4 (Cell-free assay) | 80 μM |
PDK2 (Cell-free assay) | 183 μM |