Sodium dichloroacetate is a metabolic regulator incancercells' mitochondria with anticancer activity. Sodium dichloroacetate inhibitsPDHK, resulting in decreased lactic acid in the tumor microenvironment. Sodium dichloroacetate increasesreactive oxygen species(ROS)generation and promotescancercellapoptosis. Sodium dichloroacetate also works asNKCCinhibitor^[1].

PDHK; Reactive oxygen species (ROS); Apoptosis; NKCC^[1]

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].

The NKCC1 RNA expression levels in Sodium dichloroacetate-treated gonad-intact and castrated males are significantly decreased, and no such effect is determined in the gonad-intact and castrated female Sodium dichloroacetate-treated rats^[1].
A single Sodium dichloroacetate dose causes a significantly higher 24 h diuresis in Wistar male rats, and the increased diuresis is related to NKCC2 inhibition. The NKCC2 is more abundant in kidneys of intact females compared to intact males, with a greater transporter density in Sprague-Dawley female rats^[1].
The oral Sodium dichloroacetate bioavailability in naive male rats dosed 5, 20 and 100 mg/kg is significantly lower than in GSTζ-depleted ones (10%, 13%, 81% and 31%, 75%, 100%, respectively). The liver extraction of Sodium dichloroacetate in the GSTζ-depleted rats has linear kinetics, but it decreases with the metabolism saturation at higher doses^[1].

150.92

Solid

C₂HCl₂NaO₂

2156-56-1

二氯乙酸钠

Room temperature in continental US; may vary elsewhere.

4°C, sealed storage, away from moisture

*In solvent : -80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture)

H₂O : 100 mg/mL(662.60 mM;Need ultrasonic)

请根据产品在不同溶剂中的溶解度选择合适的溶剂配制储备液；一旦配成溶液，请分装保存，避免反复冻融造成的产品失效。
储备液的保存方式和期限：-80℃, 6 months; -20℃, 1 month (sealed storage, away from moisture)。-80℃ 储存时，请在 6 个月内使用，-20℃ 储存时，请在 1 个月内使用。

请根据您的实验动物和给药方式选择适当的溶解方案。以下溶解方案都请先按照In Vitro方式配制澄清的储备液，再依次添加助溶剂：

——为保证实验结果的可靠性，澄清的储备液可以根据储存条件，适当保存；体内实验的工作液，建议您现用现配，当天使用； 以下溶剂前显示的百
分比是指该溶剂在您配制终溶液中的体积占比；如在配制过程中出现沉淀、析出现象，可以通过加热和/或超声的方式助溶

• 1.

  请依序添加每种溶剂： PBS

  Solubility: 100 mg/mL (662.60 mM); Clear solution; Need ultrasonic
• 2.

  请依序添加每种溶剂： 10% DMSO    40%PEG300   5%Tween-80   45% saline

  Solubility: ≥ 2.25 mg/mL (14.91 mM); Clear solution

  此方案可获得 ≥ 2.25 mg/mL (14.91 mM，饱和度未知) 的澄清溶液。

  以 1 mL 工作液为例，取 100 μL 22.5 mg/mL 的澄清 DMSO 储备液加到 400 μL PEG300 中，混合均匀；向上述体系中加入50 μL Tween-80，混合均匀；然后继续加入 450 μL生理盐水定容至 1 mL。

  将 0.9 g 氯化钠，完全溶解于 100 mL ddH2O 中，得到澄清透明的生理盐水溶液
• 3.

  请依序添加每种溶剂： 10% DMSO    90% (20%SBE-β-CDin saline)

  Solubility: ≥ 2.25 mg/mL (14.91 mM); Clear solution

  此方案可获得 ≥ 2.25 mg/mL (14.91 mM，饱和度未知) 的澄清溶液。

  以 1 mL 工作液为例，取 100 μL 22.5 mg/mL 的澄清 DMSO 储备液加到 900 μL20% 的 SBE-β-CD 生理盐水水溶液中，混合均匀。

  将 2 g 磺丁基醚 β-环糊精加入 5 mL 生理盐水中，再用生理盐水定容至 10 mL，完全溶解，澄清透明
• 4.

  请依序添加每种溶剂： 10% DMSO    90%corn oil

  Solubility: ≥ 2.25 mg/mL (14.91 mM); Clear solution

  此方案可获得 ≥ 2.25 mg/mL (14.91 mM，饱和度未知) 的澄清溶液，此方案不适用于实验周期在半个月以上的实验。

  以 1 mL 工作液为例，取 100 μL 22.5 mg/mL 的澄清 DMSO 储备液加到 900 μL玉米油中，混合均匀。