DCA (Sodium dichloroacetate)

Catalog No.S8615 Batch:S861505

Technical Data

Formula	C₂HCl₂O₂.Na
Molecular Weight	150.92	CAS No.	2156-56-1
Solubility (25°C)*	In vitro	DMSO	30 mg/mL (198.78 mM)
		Water	30 mg/mL (198.78 mM)
		Ethanol	30 mg/mL (198.78 mM)
* <1 mg/ml means slightly soluble or insoluble. * Please note that Selleck tests the solubility of all compounds in-house, and the actual solubility may differ slightly from published values. This is normal and is due to slight batch-to-batch variations. * Room temperature shipping (Stability testing shows this product can be shipped without any cooling measures.)

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Biological Activity

Description

DCA (Sodium dichloroacetate), a specific inhibitor of pyruvate dehydrogenase kinase (PDK) with IC50 values of 183 and 80 μM for PDK2 and PDK4 respectively, has been shown to derepress Na⁺-K⁺-2Cl^- cotransporter and a mitochondrial potassium-ion channel axis. Sodium dichloroacetate increases reactive oxygen species (ROS) generation, triggers apoptosis in cancer cells, and inhibits tumor growth.

Targets

PDK4 ^[4] (Cell-free assay)	PDK2 ^[4] (Cell-free assay)
80 μM	183 μM

In vitro

DCA can trigger apoptosis of human lung, breast and brain cancer cells^[1]. After DCA treatment, cancer cells shows increased levels of ROS, depolarization of the MMP in vitro and increased apoptosis both in vitro and in vivo^[2]. DCA inhibits the activity of pyruvate dehydrogenase kinase (PDK), thereby stimulating the mitochondrial enzyme pyruvate dehydrogenase (PDH). When turned off, PDH no longer converts pyruvate to acetyl-CoA required for mitochondrial respiration and glucose dependent oxidative phosphorylation. DCA thus shifts cellular metabolism from glycolysis to glucose oxidation, decreasing the mitochondrial membrane potential gradient and helping to open mitochondrial transition pores. This metabolic switch facilitates translocation of pro-apoptotic mediators like cytochrome c (cyt c) and apoptosis inducing factor (AIF), both of which stimulate apoptosis. DCA thereby drives cancer cells to commit suicide by apoptosis^[3].

In vivo

DCA can act as a cytostatic agent in vitro and in vivo, without causing apoptosis (programmed cell death). DCA is discovered to be a safe drug with no cardiac, pulmonary, renal or bone marrow toxicity. The most serious common side effect consists of peripheral neuropathy, which is reversible. DCA has anti-cancer activity in several cancer types including colon, prostate, ovarian, neuroblastoma, lung carcinoid, cervical, endometrial, cholangiocarcinoma, sarcoma and T-cell lymphoma. Other antineoplastic actions of DCA have also been suggested. These include angiogenesis blockade, changes in expression of HIF1-α, alteration of pH regulators V-ATPase and MCT1, and other cell survival regulators such as PUMA, GLUT1, Bcl2 and p53. DCA is able to significantly reduce metastatic burden in the lungs of rats in a highly metastatic in vivo model of breast cancer^[1]. In vivo the DCA-Na treatment induces 20% survival and decreased the tumoral diameter, volume and weight, without affect the body weight and avoid metastasis in C57BL/6 mice^[3].

Protocol (from reference)

Cell Assay:^{^[2]}	Cell lines breast cancer cell Concentrations 5 mM Incubation Time 24-72 h Method For the assessment of cell viability, cells are plated in 96 well plates at a density of 3000 cells per well and 8 wells per group. Following exposure to DCA and ATO for 24 to 72 hours, cells are incubated for 3 hours with neutral red (30 μg/ml) in fresh media, then washed with PBS, followed by the addition of lysis buffer (acetic acid/methanol, 80%/20%) and the absorbance at 540 nm is recorded. Results are expressed as mean ± S.D, calculations are performed using the Prism software package, ANOVA with Tukey post test was applied and P < 0.05 was considered to be statistically significant.
Animal Study:^{^[3]}	Animal Models C57BL/6 mice Dosages 500 and 1000 mg/kg Administration i.p.

Cell Assay:^{^[2]}

Cell lines
breast cancer cell
Concentrations
5 mM
Incubation Time
24-72 h
Method
For the assessment of cell viability, cells are plated in 96 well plates at a density of 3000 cells per well and 8 wells per group. Following exposure to DCA and ATO for 24 to 72 hours, cells are incubated for 3 hours with neutral red (30 μg/ml) in fresh media, then washed with PBS, followed by the addition of lysis buffer (acetic acid/methanol, 80%/20%) and the absorbance at 540 nm is recorded. Results are expressed as mean ± S.D, calculations are performed using the Prism software package, ANOVA with Tukey post test was applied and P < 0.05 was considered to be statistically significant.

Animal Study:^{^[3]}

Animal Models
C57BL/6 mice
Dosages
500 and 1000 mg/kg
Administration
i.p.

References

[4] Tso SC, et al. J Biol Chem. 2014, 289(7):4432-43.

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Selleck's DCA (Sodium dichloroacetate) has been cited by 13 publications

Proteomic analysis identifies PFKP lactylation in SW480 colon cancer cells [ iScience, 2024, 27(1):108645]	PubMed: 38155775
PDHA1 hyperacetylation-mediated lactate overproduction promotes sepsis-induced acute kidney injury via Fis1 lactylation [ Cell Death Dis, 2023, 14(7):457]	PubMed: 37479690
Zebrafish imaging reveals TP53 mutation switching oncogene-induced senescence from suppressor to driver in primary tumorigenesis [ Nat Commun, 2022, 13(1):1417]	PubMed: 35304872
Vps33B controls Treg cell suppressive function through inhibiting lysosomal nutrient sensing complex-mediated mTORC1 activation [ Cell Rep, 2022, 39(11):110943]	PubMed: 35705052
Reversing tozasertib resistance in glioma through inhibition of pyruvate dehydrogenase kinases [ Mol Oncol, 2022, 16(1):219-249]	PubMed: 34058053
Targeting the Hippo/YAP/TAZ signalling pathway: Novel opportunities for therapeutic interventions into skin cancers [ Exp Dermatol, 2022, 31(10):1477-1499]	PubMed: 35913427
Deacetylation of ATG4B promotes autophagy initiation under starvation [ Sci Adv, 2022, 8(31):eabo0412]	PubMed: 35921421
Cancer-associated fibroblasts promote the survival of irradiated nasopharyngeal carcinoma cells via the NF-κB pathway [ J Exp Clin Cancer Res, 2021, 40(1):87]	PubMed: 33648530
PDK4 dictates metabolic resistance to ferroptosis by suppressing pyruvate oxidation and fatty acid synthesis [ Cell Rep, 2021, 34(8):108767]	PubMed: 33626342
PDK4-mediated metabolic reprogramming is involved in rituximab resistance in DLBCL via affecting the expression of MS4A1/CD20 [ Cancer Sci, 2021, 10.1111/cas.15055]	PubMed: 34252986

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