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Chemistry

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Also known as: 148-18-5, Ditiocarb sodium, Sodium n,n-diethyldithiocarbamate, Dithiocarb, Thiocarb, Imuthiol
Molecular Formula
C5H10NNaS2
Molecular Weight
171.3  g/mol
InChI Key
IOEJYZSZYUROLN-UHFFFAOYSA-M
FDA UNII
A5304YEB5E

Ditiocarb
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.
1 2D Structure

Ditiocarb

2 Identification
2.1 Computed Descriptors
2.1.1 IUPAC Name
sodium;N,N-diethylcarbamodithioate
2.1.2 InChI
InChI=1S/C5H11NS2.Na/c1-3-6(4-2)5(7)8;/h3-4H2,1-2H3,(H,7,8);/q;+1/p-1
2.1.3 InChI Key
IOEJYZSZYUROLN-UHFFFAOYSA-M
2.1.4 Canonical SMILES
CCN(CC)C(=S)[S-].[Na+]
2.2 Other Identifiers
2.2.1 UNII
A5304YEB5E
2.3 Synonyms
2.3.1 MeSH Synonyms

1. Ammonium Salt Ditiocarb

2. Bismuth Salt Ditiocarb

3. Diethylcarbamodithioic Acid

4. Diethyldithiocarbamate

5. Diethyldithiocarbamate, Sodium

6. Diethyldithiocarbamate, Zinc

7. Diethyldithiocarbamic Acid

8. Dithiocarb

9. Ditiocarb

10. Ditiocarb Sodium

11. Ditiocarb, Ammonium Salt

12. Ditiocarb, Bismuth Salt

13. Ditiocarb, Lead Salt

14. Ditiocarb, Potassium Salt

15. Ditiocarb, Sodium Salt

16. Ditiocarb, Sodium Salt, Trihydrate

17. Ditiocarb, Tin(4+) Salt

18. Ditiocarb, Zinc Salt

19. Imuthiol

20. Lead Salt Ditiocarb

21. Potassium Salt Ditiocarb

22. Sodium Salt Ditiocarb

23. Sodium, Ditiocarb

24. Thiocarb

25. Zinc Diethyldithiocarbamate

26. Zinc Salt Ditiocarb

2.3.2 Depositor-Supplied Synonyms

1. 148-18-5

2. Ditiocarb Sodium

3. Sodium N,n-diethyldithiocarbamate

4. Dithiocarb

5. Thiocarb

6. Imuthiol

7. Dedtc

8. Sodium Diethylcarbamodithioate

9. Dedc

10. Ditiocarb Sodium [inn]

11. Ddtc

12. Carbamodithioic Acid, Diethyl-, Sodium Salt

13. Diethyldithiocarbamate Sodium

14. Cupral

15. Diethyldithiocarbamic Acid, Sodium Salt

16. Sodium Dedt

17. N,n-diethyldithiocarbamic Acid, Sodium Salt

18. A5304yeb5e

19. Sodium N,n-diethyldithiocarbamate (25% Solution In Water)

20. Usaf Ek-2596

21. Chebi:82587

22. Diethyldithiocarbamic Acid Sodium Salt

23. Diethyl Sodium Dithiocarbamate

24. Nsc-38583

25. Nci Co2835

26. Carbamodithioic Acid, N,n-diethyl-, Sodium Salt (1:1)

27. Sodium Diethylaminocarbodithioate

28. Diethyldithiocarbamic Acid, Sodium

29. Gs 694a

30. Diethyl Dithiocarbamate Sodium Salt

31. Dsstox_cid_2956

32. Dsstox_rid_76806

33. Diethylcarbamodithioic Acid, Sodium Salt

34. Dsstox_gsid_22956

35. N,n-diethyl(sodiosulfanyl)carbothioamide

36. Sodium Salt Of N,n-diethyldithiocarbamic Acid

37. Kupral

38. Dtc

39. Ditiocarbo Sodico

40. Na-ddtc

41. Nocceler Sdc

42. Chembl107217

43. Soxinol Esl

44. Ditiocarbe Sodique

45. Nsc4857

46. Cas-148-18-5

47. Ditiocarbum Natricum

48. Ncgc00166328-01

49. Ditiocarbe Sodique [french]

50. Ditiocarbo Sodico [spanish]

51. Unii-a5304yeb5e

52. Ditiocarbum Natricum [latin]

53. Ccris 235

54. Hsdb 4091

55. Einecs 205-710-6

56. Nsc 38583

57. Sodium (diethylcarbamothioyl)sulfanide

58. Ai3-14688

59. Carbamic Acid, Diethyldithio-, Sodium Salt

60. Ec 205-710-6

61. Sodiumdiethylcarbamodithioate

62. Ditiocarb Sodium [mi]

63. Schembl168133

64. Ditiocarb Sodium [hsdb]

65. Dtxsid3022956

66. Ditiocarb Sodium [mart.]

67. Ditiocarb Sodium [who-dd]

68. Sodium;n,n-diethylcarbamodithioate

69. Hy-b1637

70. Tox21_112412

71. Tox21_200403

72. Mfcd00066667

73. Akos015897389

74. Akos016358586

75. Akos025310122

76. Ncgc00257957-01

77. As-12092

78. Sodium Diethyldithiocarbamate [iarc]

79. Cs-0013580

80. Ft-0631848

81. C19599

82. D78053

83. Q413008

84. J-008449

85. F8880-1809

86. Z1522566622

2.4 Create Date
2005-03-27
3 Chemical and Physical Properties
Molecular Weight 171.3 g/mol
Molecular Formula C5H10NNaS2
Hydrogen Bond Donor Count0
Hydrogen Bond Acceptor Count2
Rotatable Bond Count2
Exact Mass171.01523595 g/mol
Monoisotopic Mass171.01523595 g/mol
Topological Polar Surface Area36.3 Ų
Heavy Atom Count9
Formal Charge0
Complexity83
Isotope Atom Count0
Defined Atom Stereocenter Count0
Undefined Atom Stereocenter Count0
Defined Bond Stereocenter Count0
Undefined Bond Stereocenter Count0
Covalently Bonded Unit Count2
4 Drug and Medication Information
4.1 Therapeutic Uses

Adjuvants, Immunologic; Antiviral Agents; Chelating Agents

National Library of Medicine's Medical Subject Headings. Ditiocarb. Online file (MeSH, 2016). Available from, as of August 12, 2016: https://www.nlm.nih.gov/mesh/2016/mesh_browser/MBrowser.html


/CLINICAL TRIALS/ ClinicalTrials.gov is a registry and results database of publicly and privately supported clinical studies of human participants conducted around the world. The Web site is maintained by the National Library of Medicine (NLM) and the National Institutes of Health (NIH). Each ClinicalTrials.gov record presents summary information about a study protocol and includes the following: Disease or condition; Intervention (for example, the medical product, behavior, or procedure being studied); Title, description, and design of the study; Requirements for participation (eligibility criteria); Locations where the study is being conducted; Contact information for the study locations; and Links to relevant information on other health Web sites, such as NLM's MedlinePlus for patient health information and PubMed for citations and abstracts for scholarly articles in the field of medicine. Sodium Diethyldithiocarbamate is included in the database.

NIH/NLM; ClinicalTrials.Gov. Available from, as of March 17, 2016: https://clinicaltrials.gov/ct2/results?term=SODIUM+DIETHYLDITHIOCARBAMATE&Search=Search


/EXPL THER/ A brief historical resume is presented on the use of dithiocarbamates for the treatment of persons exposed to nickel carbonyl. The specificity of the treatment is demonstrated in an industrial accident in which four men were simultaneously exposed to nickel carbonyl vapors. Three of the men received dithiocarb within 24 hours after exposure and the fourth was hospitalized by his family physician and treated for bronchopneumonia with antibiotics and without benefit of dithiocarb. The three workmen who received dithiocarb became symptomless and returned to work within 72 hours after exposure. The fourth man who had not received dithiocarb died within five days after exposure.

PMID:217297 Sunderman FW; Ann Clin Lab Sci. 9 (1): 1-10 (1979)


/EXPL THER/ We randomized 389 symptomatic patients with human immunodeficiency virus (HIV) infection to ditiocarb sodium (400 mg/cu m orally for 24 weeks) or a placebo. Patients were well balanced according to Centers for Disease Control (CDC) group, CD4+ cell number, and duration of disease prior to entry. Ten new acquired immunodeficiency syndrome (AIDS)-defining opportunistic infections occurred in the treated patients and 21 in the controls. Reduction of new opportunistic infections in the ditiocarb group was significant in all patients (relative risk [RR], 0.44) and in patients with AIDS (CDC groups IV-C1 and IV-D) (RR, 0.12). The size of the effect of ditiocarb was maintained when data were reanalyzed after exclusion of a patient who progressed to Pneumocystis carinii pneumonia who was not strictly CDC-defined (RR, 0.46), or when considering as new opportunistic infections three events, which were clinically active at entry, but for which the definitive diagnosis was made during study (RR, 0.49). The administration of ditiocarb did not induce any major adverse clinical or biological reactions. We conclude that, in this study, ditiocarb was safe and reduced the incidence of opportunistic infections in patients with symptomatic HIV infection.

PMID:1671884 Hersh EM et al; JAMA. 265 (12): 1538-44 (1991)


For more Therapeutic Uses (Complete) data for SODIUM DIETHYLDITHIOCARBAMATE (10 total), please visit the HSDB record page.


5 Pharmacology and Biochemistry
5.1 MeSH Pharmacological Classification

Chelating Agents

Chemicals that bind to and remove ions from solutions. Many chelating agents function through the formation of COORDINATION COMPLEXES with METALS. (See all compounds classified as Chelating Agents.)


Adjuvants, Immunologic

Substances that augment, stimulate, activate, potentiate, or modulate the immune response at either the cellular or humoral level. The classical agents (Freund's adjuvant, BCG, Corynebacterium parvum, et al.) contain bacterial antigens. Some are endogenous (e.g., histamine, interferon, transfer factor, tuftsin, interleukin-1). Their mode of action is either non-specific, resulting in increased immune responsiveness to a wide variety of antigens, or antigen-specific, i.e., affecting a restricted type of immune response to a narrow group of antigens. The therapeutic efficacy of many biological response modifiers is related to their antigen-specific immunoadjuvanticity. (See all compounds classified as Adjuvants, Immunologic.)


Antiviral Agents

Agents used in the prophylaxis or therapy of VIRUS DISEASES. Some of the ways they may act include preventing viral replication by inhibiting viral DNA polymerase; binding to specific cell-surface receptors and inhibiting viral penetration or uncoating; inhibiting viral protein synthesis; or blocking late stages of virus assembly. (See all compounds classified as Antiviral Agents.)


5.2 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.

Baselt RC, Hanson VW; Res Commun Chem Patbol Pharmacol 38 (1): 113-24 (1982) as cited in USEPA; Health and Environmental Effects Profile for Sodium Diethyldithiocarbamate p.7 (1983) ECAO-CIN-016


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.

Craven MR et al; J Pharm Pharmacol 28 (Suppl): 38 (1976) as cited in USEPA; Health and Environmental Effects Profile for Sodium Diethyldithiocarbamate p.7 (1983) ECAO-016


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.

Stromme JH; Biochem Pharmacol 14: 393-410 (1965) as cited in USEPA; Health and Environmental Effects Profile for Sodium Diethyldithiocarbamate p.7 (1983) ECAO-CIN-016


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.

Stromme JH; Biochem Pharmacol 14: 393-410 (1965) as cited in USEPA; Health and Environmental Effects Profile for Sodium Diethyldithiocarbamate p.7 (1983) ECAO-CIN-016


For more Absorption, Distribution and Excretion (Complete) data for SODIUM DIETHYLDITHIOCARBAMATE (7 total), please visit the HSDB record page.


5.3 Metabolism/Metabolites

In rats, four metabolites, diethyldithiocarbamate, diethyldithiocarbamate-s-glucuronide, inorganic sulfate and carbon disulfide were identified; these are also metabolites of disulfiram.

IARC. Monographs on the Evaluation of the Carcinogenic Risk of Chemicals to Humans. Geneva: World Health Organization, International Agency for Research on Cancer, 1972-PRESENT. (Multivolume work). Available at: https://monographs.iarc.fr/ENG/Classification/index.php, p. V12 221 (1976)


5.4 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.

PMID:20826547 Full text: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2993453 Pratt-Hyatt M et al; Drug Metab Dispos 38 (12): 2286-92 (2010)


... 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.

PMID:11212946 Tatrai E et al; J Toxicol Environ Health A 62 (3): 207-16 (2001)


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