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Technical details about Triclocarban, learn more about the structure, uses, toxicity, action, side effects and more

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2D Structure
Also known as: 101-20-2, 1-(4-chlorophenyl)-3-(3,4-dichlorophenyl)urea, 3,4,4'-trichlorocarbanilide, Solubacter, Cutisan, Procutene
Molecular Formula
C13H9Cl3N2O
Molecular Weight
315.6  g/mol
InChI Key
ICUTUKXCWQYESQ-UHFFFAOYSA-N
FDA UNII
BGG1Y1ED0Y

Triclocarban is a triclosan analogue with an antibacterial property. Triclocarban exerts its effect by inhibiting the activity of enoyl-(acyl-carrier protein) (ACP) reductase, widely distributed in bacteria, fungi and plants. ACP reductase catalyses the last step in each cycle of fatty acid elongation in the type II fatty acid synthase systems. As a result, this agent interrupts cell membrane synthesis and leads to bacterial growth inhibition.
1 2D Structure

2D Structure

2 Identification
2.1 Computed Descriptors
2.1.1 IUPAC Name
1-(4-chlorophenyl)-3-(3,4-dichlorophenyl)urea
2.1.2 InChI
InChI=1S/C13H9Cl3N2O/c14-8-1-3-9(4-2-8)17-13(19)18-10-5-6-11(15)12(16)7-10/h1-7H,(H2,17,18,19)
2.1.3 InChI Key
ICUTUKXCWQYESQ-UHFFFAOYSA-N
2.1.4 Canonical SMILES
C1=CC(=CC=C1NC(=O)NC2=CC(=C(C=C2)Cl)Cl)Cl
2.2 Other Identifiers
2.2.1 UNII
BGG1Y1ED0Y
2.3 Synonyms
2.3.1 MeSH Synonyms

1. 3,4,4'-trichlorocarbanilide

2. Cutisan

3. Septivon

4. Septivon-lavril

5. Solubacter

6. Trichlorcarban

7. Trichlorocarbanilide

2.3.2 Depositor-Supplied Synonyms

1. 101-20-2

2. 1-(4-chlorophenyl)-3-(3,4-dichlorophenyl)urea

3. 3,4,4'-trichlorocarbanilide

4. Solubacter

5. Cutisan

6. Procutene

7. Genoface

8. Trilocarban

9. Cusiter

10. N-(4-chlorophenyl)-n'-(3,4-dichlorophenyl)urea

11. Trichlorocarbanilide

12. 3,4,4'-trichlorodiphenylurea

13. Triclocarbanum

14. Urea, N-(4-chlorophenyl)-n'-(3,4-dichlorophenyl)-

15. Nsc-72005

16. Tcc

17. 3,4,4'-trichloro Carbanilide

18. 1-(3',4'-dichlorophenyl)-3-(4'-chlorophenyl)urea

19. 3,4,4-trichlorocarbanilide

20. Ent 26925

21. Cp 78416

22. N-(3,4-dichlorophenyl)-n'-(4-chlorophenyl)urea

23. Carbanilide, 3,4,4'-trichloro-

24. Nsc 72005

25. Bgg1y1ed0y

26. 3-(4-chlorophenyl)-1-(3,4-dichlorophenyl)urea

27. Trichlocarban

28. Chebi:48347

29. Nsc72005

30. Ncgc00164034-01

31. Dsstox_cid_6214

32. Dsstox_rid_78062

33. Dsstox_gsid_26214

34. Tcc Soap

35. Caswell No. 874

36. Tcc (soap Bacteriostat)

37. Triclocarban [usan:inn]

38. Triclocarbanum [inn-latin]

39. Cas-101-20-2

40. Ccris 4880

41. Hsdb 5009

42. Einecs 202-924-1

43. Unii-bgg1y1ed0y

44. Epa Pesticide Chemical Code 027901

45. Brn 2814890

46. Ai3-26925

47. (triclocarban)

48. Nipaguard Tcc

49. 9eg

50. Mfcd00013254

51. Urea,4-dichlorophenyl)-

52. Triclocarban (usp/inn)

53. Triclocarban [mi]

54. Urea-based Compound, 11

55. Triclocarban [inn]

56. 3,4'-trichlorocarbanilide

57. Ec 202-924-1

58. Triclocarban [hsdb]

59. Triclocarban [inci]

60. Triclocarban [usan]

61. 3,4'-trichlorodiphenylurea

62. Cid_7547

63. Nciopen2_008923

64. Schembl68658

65. Triclocarban [mart.]

66. Wln: Gr Dmvmr Cg Dg

67. 4-12-00-01265 (beilstein Handbook Reference)

68. Mls002415563

69. Carbanilide,4,4'-trichloro-

70. Triclocarban [usp-rs]

71. Triclocarban [who-dd]

72. 3,4,4 Inverted Exclamation Marka-trichlorocarbanilide

73. Chembl1076347

74. Dtxsid4026214

75. Bdbm25730

76. Triclocarban, Analytical Standard

77. 3,?4,?4'-?trichlorocarbanilide

78. Zinc121480

79. Hy-b1805

80. Tox21_112078

81. Tox21_202030

82. Tox21_300481

83. Triclocarban [usp Monograph]

84. S6444

85. Stk730440

86. 3,4,4'-trichlorocarbanilide, 99%

87. Akos001713711

88. Tox21_112078_1

89. Cs-7760

90. Db11155

91. Ks-5290

92. Triclocarban 100 Microg/ml In Methanol

93. Ncgc00164034-02

94. Ncgc00164034-03

95. Ncgc00164034-04

96. Ncgc00164034-05

97. Ncgc00254243-01

98. Ncgc00259579-01

99. Ac-12602

100. Smr001339078

101. 3,4,4'-trichlorocarbanilide(triclocarban)

102. Triclocarban 100 Microg/ml In Acetonitrile

103. Ft-0614114

104. T1015

105. D06223

106. E77179

107. 1-(4-chlorophenyl)-1-(3,4-dichlorophenyl)urea

108. A800352

109. Q416579

110. Sr-01000860289

111. N-(4-chlorophenyl)-n'-(3,4-dichlorophenyl)-urea

112. Q-201865

113. Sr-01000860289-2

114. Us8815951, 3-(4-chlorophenyl)-1-(3,4-dichlorophenyl)urea

115. Triclocarban, United States Pharmacopeia (usp) Reference Standard

116. 3,4,4` Trichlorocarbanilide (triclocarban), Pharmaceutical Secondary Standard; Certified Reference Material

2.4 Create Date
2005-03-26
3 Chemical and Physical Properties
Molecular Weight 315.6 g/mol
Molecular Formula C13H9Cl3N2O
XLogP35.3
Hydrogen Bond Donor Count2
Hydrogen Bond Acceptor Count1
Rotatable Bond Count2
Exact Mass313.978046 g/mol
Monoisotopic Mass313.978046 g/mol
Topological Polar Surface Area41.1 Ų
Heavy Atom Count19
Formal Charge0
Complexity308
Isotope Atom Count0
Defined Atom Stereocenter Count0
Undefined Atom Stereocenter Count0
Defined Bond Stereocenter Count0
Undefined Bond Stereocenter Count0
Covalently Bonded Unit Count1
4 Drug and Medication Information
4.1 Therapeutic Uses

Antiseptic, disinfectant.

O'Neil, M.J. (ed.). The Merck Index - An Encyclopedia of Chemicals, Drugs, and Biologicals. Cambridge, UK: Royal Society of Chemistry, 2013., p. 1789


/EXPL THER/ The increasing use of the antimicrobial triclocarban in personal care products has resulted in concern regarding environmental pollution. Triclocarban is a potent inhibitor of soluble epoxide hydrolase (sEH). Inhibitors of sEH (sEHIs) are anti-inflammatory, anti-hypertensive and cardio-protective in multiple animal models. However, the in vivo effects anticipated from a sEHI have not been reported for triclocarban. Here we demonstrated the anti-inflammatory effects in vivo of triclocarban in a murine model. Triclocarban was employed in a lipopolysaccharide (LPS)-challenged murine model. Systolic blood pressure, plasma levels of several inflammatory cytokines and chemokine, and metabolomic profile of plasma oxylipins were determined. Triclocarban significantly reversed LPS-induced morbid hypotension in a time-dependent manner. Triclocarban significantly repressed the increased release of inflammatory cytokines and chemokine caused by LPS. Furthermore, triclocarban significantly shifted the oxylipin profile in vivo in a time-dependent manner towards resolution of inflammation as expected from a sEHI. These results demonstrated that at the doses used triclocarban is anti-inflammatory in the murine model. This study suggests that triclocarban may provide some benefits in humans in addition to its antimicrobial activities due to its potent inhibition of sEH. It may be a promising starting point for developing new low volume high value applications of triclocarban. However these biological effects also caution against the general over use of triclocarban in personal care products.

PMID:21741984 Full text: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3156297 Liu JY et al; Toxicol Appl Pharmacol 255 (2): 200-6 (2011)


4.2 Drug Indication

Triclocarban (TCC), or 3,4,4'-trichlorocarbanilide, is an antibacterial agent used in bar and liquid soaps and body washes.


5 Pharmacology and Biochemistry
5.1 Pharmacology

The antimicrobial mechanism underlying the bacteriostatic and bactericidal effects of triclocarban is believed to be an unspecific adsorption to cell membranes and interruption of their function. As a result, the growth of gram-positive as well as gram-negative bacteria is inhibited.


5.2 MeSH Pharmacological Classification

Anti-Infective Agents, Local

Substances used on humans and other animals that destroy harmful microorganisms or inhibit their activity. They are distinguished from DISINFECTANTS, which are used on inanimate objects. (See all compounds classified as Anti-Infective Agents, Local.)


Water Pollutants, Chemical

Chemical compounds which pollute the water of rivers, streams, lakes, the sea, reservoirs, or other bodies of water. (See all compounds classified as Water Pollutants, Chemical.)


5.3 Absorption, Distribution and Excretion

Absorption

A human exposure study in a small group of subjects demonstrated that a portion of the TCC present in bar soaps is absorbed through the skin and is excreted in urine as N-glucuronides. Because they are produced and used in large quantities in various products, they are absorbed into the human body of the general population. The absorption of triclocarban during a human pharmacokinetic study was estimated at 0.6% of the 70 + or - 15 mg of triclocarban in the soap used. The triclocarban-N-glucuronide urine concentration varied considerably among the study subjects, and continuous daily use of the soap led to steady-state levels of excretion.


Route of Elimination

The metabolism of (14)C-TCC (3,4,4'-trichlorocarbanilide) has been investigated in humans following oral exposure to 2.2 mumol/kg. Fecal elimination (70% of dose) was complete at the 120 hour point after administration and the urinary excretion (27% of dose) was complete after 80 hours post-administration. Urinary glucuronides appear to be valuable biomarkers of triclocarban exposure.


Clearance

After a pharmacokinetic study in man, radioactivity was rapidly cleared from blood after intravenous administrations of (14)C-triclocarban in propylene glycol with a blood clearance half-life measured to be 8.6 hours.


/MILK/ ... Sprague Dawley rats were provided control, 0.2% weight/weight (w/w), or 0.5% w/w TCC-supplemented chow through a series of 3 experiments that limited exposure to critical growth periods: gestation, gestation and lactation, or lactation only (cross-fostering) to determine the susceptible windows of exposure for developmental consequences. ... The average concentration of TCC in the milk was almost 4 times that of the corresponding maternal serum levels. The results demonstrate that gestational TCC exposure does not affect the ability of dams to carry offspring to term but TCC exposure during lactation has adverse consequences on the survival of offspring although the mechanism of reduced survival is currently unknown. This information highlights the importance of evaluating the safety of TCC application in personal care products and the impacts during early life exposure.

PMID:24803507 Full text: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4527418 Kennedy RC et al; Reprod Sci 22 (1): 75-89 (2015)


The antibacterial triclocarban (TCC) concentrates in the cellular fraction of blood. Consequently, plasma levels are at least two-fold lower than the TCC amount present in blood. Utilizing whole blood sampling, a low but significant absorption of TCC from soap during showering is demonstrated for a small group of human subjects.

PMID:22273184 Full text: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3538789 Schebb NH et al; Chemosphere 87 (7): 825-7 (2012)


The route and rate of excretion by rats of the germicide (14)C-triclocarban formerly called trichlorocarbanilide, given by parenteral injection has been investigated. Blood levels based on radioactivity and by chemical determination after parenteral injection have been compared with those obtained after topical application of (14)C-triclocarban in soaps and in dimethylformamide (DMF) through occluded rat skin has been studied. Other soaps and a hand cleanser containing (14)C-triclocarban have been applied to rat skin without occlusion and the effects of duration of contact, concentration and the use of a solubilizer have been investigated. In humans, absorption of triclocarban through skin after bathing daily for 28 days has been investigated by chemical analysis of blood and urine. The data show that elimination by the rat is rapid and complete principally via the feces. Blood levels after parenteral injection are low and comparison of the radioactivity and chemical determinations suggest rapid metabolism of the Triclocarban. After application to the skin, blood levels based on (14)C-triclocarban are very low. Absorption of (14)C-triclocarban through occluded rat skin was greater from DMF than from soaps. With non-occluded rat skin, absorption from soaps was less and was dependent on concentration but independent of duration of contact. The use of a solubilizer did not increase absorption through skin. No measurable triclocarban (less than 25 ppb) was present in blood and urine samples of volunteers during or shortly after a 28-day intensive bathing regimen.

PMID:941165 Howes D, Black JG; Toxicology 6 (1): 67-76 (1976)


The metabolism and disposition of (14)C-TCC (3,4,4'-trichlorocarbanilide) have been evaluated in humans following oral exposure to 2.2 umol/kg body wt. Fecal elimination (70% of dose) was complete 120 hr after dosing and the urinary excretion (27% of dose) was completed in 80 hr. The maximum plasma level occurred 2.8 hr after dosing and was 3.7 nmol-equivalents of TCC per g of plasma (approximately 1.2 ppm). Biotransformation of TCC was rapid but did not appear to involve splitting of the basic TCC structure. The major plasma metabolites were N- and N'-glucuronides of TCC which were eliminated with half life approximately 2 hr to the urine and 2'-hydroxy-TCC sulfate and 6-hydroxy-TCC sulfate (the o-hydroxy-TCC sulfates) which were removed with half life approximately 20 hr (presumably into the bile). ...

PMID:26534 Hiles RA, Birch CG; Drug Metab Dispos 6 (2): 177-83 (1978)


For more Absorption, Distribution and Excretion (Complete) data for Triclocarban (10 total), please visit the HSDB record page.


5.4 Metabolism/Metabolites

Blood levels after parenteral injection are low and comparison of the radioactivity and chemical determinations suggest rapid metabolism of the Triclocarban. Human metabolism of TCC involves direct glucuronidation to form N- and N'- glucuronides as well as ring hydroxylation to 2'-hydroxy-TCC and 6-hydroxy-TCC, which are further metabolized to sulfate and glucuronide conjugates. In human subjects given a single oral dose of TCC, 27% of the dose was excreted in the urine within 80 hours. About 70% of the administered dose was excreted in the feces within 5 days. The major urinary metabolites were N-glucuronides (average levels, 30 ng/mL) and a major plasma metabolite was the sulfate conjugate of 2'-OH-TCC (levels ranged from 0-20 ng/mL. The maximum plasma level occurred 2.8 hr after dosing and was 3.7 nmol-equivalents of TCC per g of plasma (approximately 1.2 ppm). Biotransformation of TCC was rapid but did not appear to involve splitting of the basic TCC structure. The major plasma metabolites were N- and N'-glucuronides of TCC which were eliminated with half-life approximately 2 hr to the urine and 2'-hydroxy-TCC sulfate and 6-hydroxy-TCC sulfate (the o-hydroxy-TCC sulfates) which were removed with half life approximately 20 hr (presumably into the bile).


The metabolism and disposition of (14)C-TCC (3,4,4'-trichlorocarbanilide) have been evaluated in humans following oral exposure to 2.2 umol/kg body wt. Fecal elimination (70% of dose) was complete 120 hr after dosing and the urinary excretion (27% of dose) was completed in 80 hr. ... Biotransformation of TCC was rapid but did not appear to involve splitting of the basic TCC structure. The major plasma metabolites were N- and N'-glucuronides of TCC which were eliminated with half life approximately 2 hr to the urine and 2'-hydroxy-TCC sulfate and 6-hydroxy-TCC sulfate (the o-hydroxy-TCC sulfates) which were removed with half life approximately 20 hr (presumably into the bile). ...

PMID:26534 Hiles RA, Birch CG; Drug Metab Dispos 6 (2): 177-83 (1978)


Plant uptake and metabolism of emerging organic contaminants, such as personal-care products, pose potential risks to human health. In this study, jalapeno pepper (Capsicum annuum) plants cultured in hydroponic media were exposed to both (14)C-labeled and unlabeled triclocarban (TCC) to investigate the accumulation, distribution, and metabolism of TCC following plant uptake. The results revealed that TCC was detected in all plant tissues; after 12 weeks, the TCC concentrations in root, stem, leaf, and fruit tissues were 19.74 +/- 2.26, 0.26 +/- 0.04, 0.11 +/- 0.01, and 0.03 +/- 0.01 mg/kg dry weight, respectively. More importantly, a substantial portion of the TCC taken up by plants was metabolized, especially in the stems, leaves, and fruits. Hydroxylated TCC (e.g., 2'-OH TCC and 6-OH TCC) and glycosylated OH-TCC were the main phase I and phase II metabolites in plant tissues, respectively. Bound (or nonextractable) residues of TCC accounted for approximately 44.6, 85.6, 69.0, and 47.5% of all TCC species that accumulated in roots, stems, leaves, and fruits, respectively. The concentrations of TCC metabolites were more than 20 times greater than the concentrations of TCC in the above-ground tissues of the jalapeno pepper plants after 12 weeks; crucially, approximately 95.6% of the TCC was present as metabolites in the fruits. Consequently, human exposure to TCC through the consumption of pepper fruits is expected to be substantially higher when phytometabolism is considered.

PMID:29637774 Huynh K et al; J Agric Food Chem 66 (16): 4032-4043 (2018)


Previous studies of triclocarban suggest that its biotransformation could yield reactive metabolites that form protein adducts. Since the skin is the major route of triclocarban exposure, present work examined this possibility in cultured human keratinocytes. The results provide evidence for considerable biotransformation and protein adduct formation when cytochrome P450 activity is induced in the cells by 2,3,7,8-tetrachlorodibenzo-p-dioxin, a model Ah receptor ligand. Since detecting low adduct levels in cells and tissues is difficult, we utilized the novel approach of accelerator mass spectrometry for this purpose. Exploiting the sensitivity of the method, we demonstrated that a substantial portion of triclocarban forms adducts with keratinocyte protein under the P450 inducing conditions employed.

PMID:22711420 Full text: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3522462 Schebb NH et al; J Biochem Mol Toxicol 26 (6): 230-4 (2012)


... After repeated oral administration of 3,4,4'-trichlorocarbanilide (TCC) ... the biliary metabolites ... were isolated and identified. The major TCC biliary metabolite was found to be 2'-hydroxy-TCC. This compound was isolated mainly from the nonconjugated and the glucuronide fractions. Other metabolites present in substantial quantities were 6-hydroxy-TCC and 2',6-dihydroxy-TCC mainly as glucuronides and 3'-hydroxy-TCC mainly as the sulfate conjugate. Small amounts of 3',6-dihydroxy-TCC were isolated from each of the fractions. No unchanged TCC was found in the bile. Only traces of other metabolites were found, and no N-hydroxylated products were observed. ...

PMID:15808 Jeffcoat AR Et Al; Drug Metab Dispos 5 (2): 157-66 (1977)


For more Metabolism/Metabolites (Complete) data for Triclocarban (7 total), please visit the HSDB record page.


5.5 Biological Half-Life

10 hours


The metabolism and disposition of (14)C-TCC (3,4,4'-trichlorocarbanilide) have been evaluated in humans following oral exposure to 2.2 umol/kg body wt. ... The major plasma metabolites were N- and N'-glucuronides of TCC which were eliminated with half life approximately 2 hr to the urine and 2'-hydroxy-TCC sulfate and 6-hydroxy-TCC sulfate (the o-hydroxy-TCC sulfates) which were removed with half life approximately 20 hr (presumably into the bile). ...

PMID:26534 Hiles RA, Birch CG; Drug Metab Dispos 6 (2): 177-83 (1978)


... Radioactivity was rapidly cleared from blood after intravenous administrations of (14)C-triclocarban in propylene glycol with a blood clearance half-life of 8.6 hours. About 54% of the dose was excreted in the feces and 21% of the dose in the urine with a urinary elimination half-life of ten hours. ...

PMID:1109279 Scharpf LG Jr et al; Arch Environ Health 30 (1): 7-14 (1975)


5.6 Mechanism of Action

Triclocarban is a triclosan analog with an antibacterial activity. Triclocarban exerts its effect by inhibiting the activity of _enoyl-(acyl-carrier protein) (ACP) reductase_, which is ubiquitously distributed in bacteria, fungi and various plants. ACP reductase catalyzes the last step in each cycle of fatty acid elongation in the type II fatty acid synthase systems. As a result, this agent interrupts cell membrane synthesis and leads to bacterial growth inhibition.


As a carbanilide, /triclocarban/ can be classified according to its antimicrobial mechanism as a membrane active compound. The mode of action can be described as unspecific adsorption to cell membranes, interruption of the function of interstitial proteins and/or loss of the semipermeability of the membrane, with discharge of ions and organic molecules. Bacteriostatic or bactericidal effects occur dependent on the concentration. In its standard application concentrations, triclocarban inhibits primarily the growth of gram-positive bacteria, but also that of gram-negative bacteria. Unlike antibiotics, membrane-active antimicrobial substances such as triclocarban are effective within a short period of time.

European Commission; Health & Consumer Protection Directorate-General; Scientific Committee on Consumer Products (SCCP), Opinion on Triclocarban for Other Uses Than as a Preservative, p4 (June 2005). Available from, as of May 8, 2018: https://ec.europa.eu/health/ph_risk/committees/04_sccp/docs/sccp_o_016.pdf


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