DCA (Sodium dichloroacetate)

別名：Dichloroacetic acid, bichloroacetic acid, BCA

製品コード：S8615 純度：99.90%

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.

CAS No. 2156-56-1

サイズ	価格(税別)	在庫状況
100mg	JPY 22000	国内在庫あり
1g	JPY 55500	国内在庫あり

代表番号: 045-509-1970\|電子メール：[email protected] よく尋ねられる質問

文献中Selleckの製品使用例（17）

製品安全説明書

現在のバッチを見る：純度： 99.90%

99.90

DCA (Sodium dichloroacetate)関連製品

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シグナル伝達経路

Dehydrogenaseシグナル伝達経路

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

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
実験結果図	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
臨床試験 (data from https://clinicaltrials.gov, updated on 2024-05-22)
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

参考
[1] Khan A, et al. World J Clin Cases. 2016, 4(10):336-343. [2] Sun RC, et al. Mol Cancer. 2011, 10:142. [3] Crystel Aleyvick Sierra-Rivera. African journal of microbiology research. 2012, 6(22):4782-4796. [4] Tso SC, et al. J Biol Chem. 2014, 289(7):4432-43. + 展開

参考

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

+ 展開

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	3年-20°C粉	溶液の保管冷凍と解凍の繰り返しを避けるため小分けにしてください	1年-80°Cin solvent
保管	3年-20°C粉	溶液の保管冷凍と解凍の繰り返しを避けるため小分けにしてください	1个月-20°Cin solvent

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
=	×	×

希釈計算器分子量計算器

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）

投与量 mg/kg 動物平均体重 g 投与体積（動物毎）μL 動物数匹

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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