The cementation rate is increased when copper diethyldithiocarbamate complex is formed by the reaction of sodium dithiocarb (sodium diethyldithiocarbamate) with Cu2+ solution [1]. An compound with potent antioxidant and chelating properties is sodium dithiocarb [2].

Aged and neonatal mice with suppressed immune responses benefit from sodium dithiocarb (sodium diethyldithiocarbamate). Without lowering antitumor activity, sodium diethyldithiocarbamate shields animals from cisplatin nephrotoxicity. Dithiocarb sodium is able to improve immunity, prolong survival, and lessen lymphadenopathy and hypergammaglobulinemia in AIDS models [2].

Absorption, Distribution and Excretion
Rats were administered 500 mg of dithiocarbamate (dissolved in 1-2 mL/kg body weight of water) by gavage. Within 3 hours, the plasma concentration of dithiocarbamate reached 2 mg/L. S-dithiocarbamate dissolved in 2M phosphate buffer was injected intraperitoneally into the small intestine of adult male Wistar rats at a dose of 25 mg/kg, and its absorption half-life was determined to be 26 minutes. Within 15 minutes after intraperitoneal injection of 25 mg (222 mol S)/rat of S-dithiocarbamate, non-protein-bound radiolabeled substances were detected in plasma (1561 nmol/mL plasma) and liver (3211 nmol/g liver). The study found that a significant proportion (>45%) of the radioactive material reversibly bound to soluble proteins in the liver and plasma within 15 minutes of administration.
A small amount (<0.1%) of unmetabolized dithiocarbamate was detected in the urine of rats that received an intraperitoneal injection of 25 mg (35)S-dithiocarbamate per rat. One hour after administration, 96.1% of the radiolabeled metabolites in the urine were S-glucuronide conjugates and 3.9% were inorganic sulfates. Within one hour after administration, 7% of the administered (35)S-dithiocarbamate was recovered from exhaled breath as carbon disulfide.
For more complete data on the absorption, distribution, and excretion of sodium diethyldithiocarbamate (7 in total), please visit the HSDB record page.

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Metabolisms/Metabolites
In rats, four metabolites were identified: diethyldithiocarbamate, diethyldithiocarbamate-S-glucuronide, inorganic sulfate, and carbon disulfide; these are also metabolites of disulfiram.

[1]. Sodium diethyldithiocarbamate as accelerator of the rate of copper cementation. The Egyptian Journal of Aquatic Research. 2015 Dec, Volume 41(4):289-293.

[2]. Ditiocarb sodium (diethyldithiocarbamate) therapy in patients with symptomatic HIV infection and AIDS. A randomized, double-blind, placebo-controlled, multicenter study. JAMA. 1991 Mar 27;265(12):1538-44.

[3]. Sodium dithiocarb as adjuvant immunotherapy for high risk breast cancer: a randomized study. Biotherapy. 1993;6(1):9-12.

Sodium diethyldithiocarbamate is an odorless white, slightly brown, or slightly pink crystal. (NTP, 1992)
Sodium diethyldithiocarbamate is an organic molecular entity.
Sodium dithiocarbamate is the sodium salt form of dithiocarbamate, the active metabolite of disulfiram, which has potential antitumor and chemosensitizing activities. After administration, sodium dithiocarbamate forms a complex with copper (Cu), a metal that selectively accumulates in cancer cells. This complex inhibits the nuclear factor-κB (NF-κB) pathway activated by tumor hypoxia, thereby inhibiting tumor cell growth. It may also reverse chemosensitivity and enhance the cytotoxicity of other chemotherapeutic drugs.
A chelating agent that has been used to remove toxic metals from tissues in humans and laboratory animals. It is the major metabolite of disulfiram.
Mechanism of Action

Although the ability of disulfiram to inactivate CYP2E1 has been known for over 20 years, its mechanism remains unclear. The disulfiram metabolite diethyl dithiocarbamate (DDC) is converted to an active intermediate via CYP2E1, which subsequently inactivates the CYP2E1 protein, resulting in mechanism-based inactivation. Mass spectrometry analysis of the inactivated human CYP2E1 protein revealed that inactivation is due to the formation of an adduct between the active metabolite of DDC and an apolipoprotein. These data, along with mass spectrometry analysis of the active intermediate bound to GSH, indicate the involvement of an active intermediate with a molecular weight of 116 Da. Our results suggest that this binding involves the formation of a disulfide bond with one of the eight cysteine residues in CYP2E1. This study also investigated the inactivation of wild-type CYP2E1 and its two polymorphic mutants, CYP2E12 and CYP2E14. The K(I) value for wild-type CYP2E1 was 12.2 μM, and the k(inact) value was 0.02 min⁻¹. The K(I) values of the two polymorphic mutants, CYP2E12 and CYP2E14, were 227.6 μM and 12.4 μM, respectively, and the k(inact) values were 0.0061 min⁻¹ and 0.0187 min⁻¹, respectively. These data indicate that DDC's inactivation efficiency against CYP2E1.2 is much lower than its inactivation efficiency against wild-type or CYP2E1.4 variants. DDTC significantly inhibited the activities of superoxide dismutase, gamma-glutamyl transferase, glutathione reductase, and alkaline phosphatase, while increasing the activity of glutathione peroxidase. Type II alveolar cell membranes were damaged.

C5H10NNAS2

171.25

171.015

148-18-5

Ditiocarb;147-84-2;Ditiocarb-d10 sodium;1261395-23-6

533728

White to off-white solid powder

1.086g/cm3

176.4ºC at 760mmHg

95°C

60.5ºC

1.81

0

2

2

9

83

0

[S-]C(N(C([H])([H])C([H])([H])[H])C([H])([H])C([H])([H])[H])=S.[Na+]

IOEJYZSZYUROLN-UHFFFAOYSA-M

InChI=1S/C5H11NS2.Na/c1-3-6(4-2)5(7)8;/h3-4H2,1-2H3,(H,7,8);/q;+1/p-1

sodium;N,N-diethylcarbamodithioate

Ditiocarb sodium NSC-38583 NSC38583NSC 38583

2934.99.9001

Powder      -20°C    3 years

                     4°C     2 years

In solvent   -80°C    6 months

                  -20°C    1 month

Note: Please store this product in a sealed and protected environment, avoid exposure to moisture.

Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)

DMSO : ~100 mg/mL (~583.91 mM)

Solubility in Formulation 1: ≥ 2.5 mg/mL (14.60 mM) (saturation unknown) in 10% DMSO + 40% PEG300 + 5% Tween80 + 45% Saline (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 25.0 mg/mL clear DMSO stock solution to 400 μL PEG300 and mix evenly; then add 50 μL Tween-80 to the above solution and mix evenly; then add 450 μL normal saline to adjust the volume to 1 mL.
Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH₂ O to obtain a clear solution.

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Solubility in Formulation 2: ≥ 2.5 mg/mL (14.60 mM) (saturation unknown) in 10% DMSO + 90% (20% SBE-β-CD in Saline) (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 25.0 mg/mL clear DMSO stock solution to 900 μL of 20% SBE-β-CD physiological saline solution and mix evenly.
Preparation of 20% SBE-β-CD in Saline (4°C，1 week): Dissolve 2 g SBE-β-CD in 10 mL saline to obtain a clear solution.

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Solubility in Formulation 3: ≥ 2.5 mg/mL (14.60 mM) (saturation unknown) in 10% DMSO + 90% Corn Oil (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 25.0 mg/mL clear DMSO stock solution to 900 μL of corn oil and mix evenly.

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 (Please use freshly prepared in vivo formulations for optimal results.)