DCA (Sodium dichloroacetate)

別名:Dichloroacetic acid, bichloroacetic acid, BCA

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.

DCA (Sodium dichloroacetate)化学構造

CAS No. 2156-56-1

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DCA (Sodium dichloroacetate)関連製品

Dehydrogenase阻害剤の選択性比較

Cell Data

Cell Lines Assay Type Concentration Incubation Time 活性情報 PMID
MCF7 Function assay 10 mM 12 hrs Inhibition of PDK1 in human MCF7 cells assessed as increase in oxygen consumption rate at 10 mM after 12 hrs 27006991
MCF7 Function assay 10 mM 12 hrs Inhibition of PDK1 in human MCF7 cells assessed as decrease in extracellular acidification rate at 10 mM after 12 hrs 27006991
MCF7 Function assay 10 mM 12 hrs Inhibition of PDK1 in human MCF7 cells assessed as decrease in proton production rate at 10 mM after 12 hrs 27006991
MCF7 Function assay 10 mM 12 hrs Inhibition of PDK1 in human MCF7 cells assessed as increase in ratio of oxygen consumption rate to extracellular acidification rate at 10 mM after 12 hrs 27006991
MCF7 Function assay 10 mM 12 hrs Inhibition of PDK1 in human MCF7 cells assessed as decrease in lactate production at 10 mM after 12 hrs 27006991
NCI-H1975 Antiproliferative assay 20 mM 72 hrs Antiproliferative activity against human NCI-H1975 cells assessed as reduction in cell viability at 20 mM after 72 hrs by MTT assay 30470491
MCF7 Antitumor assay 30 mg/kg two weeks Antitumor activity against human MCF7 cells xenografted in BALB/c nude mouse assessed as tumor growth inhibition at 30 mg/kg, iv administered every two days for two weeks measured after 14 days 31509699
MCF7 Function assay 30 uM 4 hrs Induction of metabolic reversal from aerobic glycolysis to oxidative phosphorylation in human MCF7 cells assessed as increase in extracellular acidification rate at 30 uM pretreated for 4 hrs followed by glucose addition after 25 mins by seahorse XF24 ext 31509699
MCF7 Function assay 30 uM 4 hrs Induction of metabolic reversal from aerobic glycolysis to oxidative phosphorylation in human MCF7 cells assessed as increase in extracellular acidification rate at 30 uM pretreated for 4 hrs followed by glucose addition after 25 mins followed by subsequent assay 31509699
MCF7 Function assay 30 uM 4 hrs Induction of metabolic reversal from aerobic glycolysis to oxidative phosphorylation in human MCF7 cells assessed as decline in extracellular acidification rate at 30 uM pretreated for 4 hrs followed by glucose addition after 25 mins followed by subsequent assay 31509699
MCF7 Function assay 30 uM 6 hrs Induction of metabolic reversal from aerobic glycolysis to oxidative phosphorylation in human MCF7 cells assessed as decrease in oxygen consumption rate at 30 uM pretreated for 6 hrs followed by oligomycin A addition after 25 mins followed by subsequent assay 31509699
MCF7 Function assay 90 mins Inhibition of PDK1 (unknown origin) expressed in human MCF7 cells using PDK tide as substrate measured after 90 mins in presence of ATP by ADP-Glo luminescent kinase assay 31509699
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生物活性

製品説明 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
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].
細胞実験 細胞株 breast cancer cell
濃度 5 mM
反応時間 24-72 h
実験の流れ

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.

実験結果図 Methods Biomarkers 結果図 PMID
Western blot pPDH E1α / PDH E1α 25630799
In Vivo
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].
動物実験 動物モデル C57BL/6 mice
投与量 500 and 1000 mg/kg
投与経路 i.p.
NCT Number Recruitment Conditions Sponsor/Collaborators Start Date Phases
NCT06073106 Not yet recruiting
Stroke|Traumatic Brain Injury|Knee Osteoarthritis|Breast Cancer
Tan Tock Seng Hospital|Rehabilitation Research Institute of Singapore (RRIS)|Woodlands Health (WH)
December 2023 --
NCT05810623 Not yet recruiting
Upper Urinary Tract Urothelial Carcinoma|Bladder Cancer
David D''Andrea|Medical University of Vienna
June 1 2023 Phase 3
NCT05646485 Recruiting
Bladder Cancer|Urothelial Carcinoma|Hematuria|Smoking Cessation
University of Texas Southwestern Medical Center
May 5 2023 Not Applicable
NCT05460533 Recruiting
B-cell Acute Lymphoblastic Leukemia
Memorial Sloan Kettering Cancer Center|Novartis Pharmaceuticals
July 12 2022 Phase 2

化学情報

分子量 150.92 化学式

C2HCl2O2.Na

CAS No. 2156-56-1 SDF Download DCA (Sodium dichloroacetate) SDFをダウンロードする
Smiles C(C(=O)[O-])(Cl)Cl.[Na+]
保管

In vitro
Batch:

モル濃度計算器

in vivo
Batch:

Add solvents to the product individually and in order.

投与溶液組成計算機

実験計算

モル濃度計算器

質量 濃度 体積 分子量

投与溶液組成計算機(クリア溶液)

ステップ1:実験データを入力してください。(実験操作によるロスを考慮し、動物数を1匹分多くして計算・調製することを推奨します)

mg/kg g μL

ステップ2:投与溶媒の組成を入力してください。(ロット毎に適した溶解組成が異なる場合があります。詳細については弊社までお問い合わせください)

% DMSO % % Tween 80 % ddH2O
%DMSO %

計算結果:

投与溶媒濃度: mg/ml;

DMSOストック溶液調製方法: mg 試薬を μL DMSOに溶解する(濃度 mg/mL, 注:濃度が当該ロットのDMSO溶解度を超える場合はご連絡ください。 )

投与溶媒調製方法:Take μL DMSOストック溶液に μL PEG300,を加え、完全溶解後μL Tween 80,を加えて完全溶解させた後 μL ddH2O,を加え完全に溶解させます。

投与溶媒調製方法:μL DMSOストック溶液に μL Corn oil,を加え、完全溶解。

注意:1.ストック溶液に沈殿、混濁などがないことをご確認ください;
2.順番通りに溶剤を加えてください。次のステップに進む前に溶液に沈殿、混濁などがないことを確認してから加えてください。ボルテックス、ソニケーション、水浴加熱など物理的な方法で溶解を早めることは可能です。

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