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 receiving levels of 500 mg of dithiocarb in 1-2 mL water/kg body weight by gavage reached plasma levels of 2 mg/L dithiocarb in 3 hours.
A half life for absorption of 26 minutes was determined when S-dithiocarb dissolved in 2M phosphate buffer was injected into the small intestinal lumen of adult male Wistar rats at a dose of 25 mg/kg.
Within 15 minutes of dosing rats with 25 mg (222 moles S)/rat S-dithiocarb i.p., nonprotein bound radiolabel was detected in the plasma (1561 nmoles/mL plasma) and in the liver (3211 nmoles/g liver). A substantial amount (>45% within 15 minutes of dosing) of radioactivity also was found to be bound reversibly to soluble proteins of liver and plasma.
A small amount (<0.1%) of unchanged dithiocarb was detected in the urine of rats receiving ip injections of 25 mg (35)S-dithiocarb/rat. One hr after dosing, 96.1% of the radiolabeled urinary metabolites was of S-glucuronide conjugate and 3.9% inorganic sulfate. Within 1 hr after dosing, 7% of the administered (35)S-dithiocarb was recovered as carbon disulfide in the expired air.
For more Absorption, Distribution and Excretion (Complete) data for SODIUM DIETHYLDITHIOCARBAMATE (7 total), please visit the HSDB record page.

---

Metabolism / Metabolites
In rats, four metabolites, diethyldithiocarbamate, diethyldithiocarbamate-s-glucuronide, inorganic sulfate and carbon disulfide were identified; 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 appears as odorless white or slightly brown or slightly pink crystals. (NTP, 1992)
Sodium diethyldithiocarbamate is an organic molecular entity.
Ditiocarb Sodium is the sodium salt form of ditiocarb, an active metabolite of disulfiram, with potential antineoplastic and chemosensitizing activities. Upon administration, ditiocarb sodium may form a complex with copper (Cu), a metal that selectively accumulates in cancer cells. This complex may inhibit the nuclear factor-kB (NF-kB) pathway activated by tumor hypoxia, thereby inhibiting tumor cell growth. It may also reverse chemoresistance and enhance cytotoxicity of other chemotherapeutic agents.
A chelating agent that has been used to mobilize toxic metals from the tissues of humans and experimental animals. It is the main metabolite of DISULFIRAM.

---

Mechanism of Action
Although the ability of disulfiram to inactivate CYP2E1 has been known for more than 20 years, the mechanism has not yet been elucidated. A metabolite of disulfiram, diethyldithocarbamate (DDC), is converted by CYP2E1 to a reactive intermediate that subsequently inactivates the protein, leading to mechanism-based inactivation. Mass spectral analysis of the inactivated human 2E1 protein demonstrates that the inactivation is due to the formation of an adduct of the reactive metabolite of DDC with the apoprotein. These data, along with mass spectral analysis of a reactive intermediate trapped with GSH, indicate the involvement of a reactive intermediate with a molecular mass of 116 Da. Our results suggest that this binding involves formation of a disulfide bond with one of the eight cysteines in CYP2E1. The inactivation of wild-type CYP2E1 as well as two of its polymorphic mutants, CYP2E1*2 and CYP2E1*4, was also investigated. For wild-type CYP2E1, the K(I) was 12.2 uM and the k(inact) was 0.02 min(-1). The K(I) values for the two polymorphic mutants were 227.6 and 12.4 uM for CYP2E1.2 and CYP2E1.4, and the k(inact) values were 0.0061 and 0.0187 min(-1), respectively. These data indicate that DDC is a much less efficient inactivator of CYP2E1.2 than it is of either the wild-type or the CYP2E1.4 variant.
... DDTC significantly inhibited the activity of superoxide dismutase and the activity of gamma-glutamyl transpeptidase, glutathione reductase, and alkaline phosphatase, whereas an increase in the activity of glutathione peroxidase was found. The membranes of pneumocytes type II were injured.

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.

---

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.

---

View More

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.

---

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