Bioactivity | Sodium dichloroacetate is a metabolic regulator in cancer cells' mitochondria with anticancer activity. Sodium dichloroacetate inhibits PDHK, resulting in decreased lactic acid in the tumor microenvironment. Sodium dichloroacetate increases reactive oxygen species (ROS) generation and promotes cancer cell apoptosis. Sodium dichloroacetate also works as NKCC inhibitor[1]. |
Invitro | Sodium dichloroacetate increases ROS generation in mitochondria. Sodium dichloroacetate affects cell growth and viability through the ROS production increase derived from the promotion of oxidative metabolism. The effects of Sodium dichloroacetate on multiple myeloma cell viability, cell cycle arrest, and apoptotic cell death were associated with pyruvate dehydrogenase kinases (PDK) inhibition, restored pyruvate dehydrogenase (PDH) activity, and the promotion of oxidative metabolism in association with increased intracellular ROS production which depends on the Sodium dichloroacetate dose. The Sodium dichloroacetate effects cooperated with C I inhibition promoting the oxidative stress in rat VM-M3 glioblastoma cells. Increased ROS levels in Sodium dichloroacetate-treated cancer cells are related to the induction of apoptosis associated with the increased cytochrome c expression. Sodium dichloroacetate causes ROS-dependent T-cell differentiation[1]. |
Name | Sodium dichloroacetate |
CAS | 2156-56-1 |
Formula | C2HCl2NaO2 |
Molar Mass | 150.92 |
Transport | Room temperature in continental US; may vary elsewhere. |
Storage | 4°C, sealed storage, away from moisture *In solvent : -80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture) |