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Chemical Compound Review

Manusept     5-chloro-2-(2,4- dichlorophenoxy)phenol

Synonyms: Sapoderm, triclosan, Cliniclean, Trisan, Microshield T, ...
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Disease relevance of triclosan


Psychiatry related information on triclosan

  • This investigation examined the antimicrobial effects of a new liquid triclosan/copolymer dentifrice (test) formulation that demonstrated significant inhibition of oral malodor in previous organoleptic clinical studies [6].

High impact information on triclosan

  • The antimicrobial biocide triclosan [5-chloro-2-(2,4-dichlorophenoxy)phenol] potently inhibits the growth of Plasmodium falciparum in vitro and, in a mouse model, Plasmodium berghei in vivo [7].
  • Transferable resistance to triclosan in MRSA [8].
  • Humans, the vertebrate host for the malarial parasite utilize type I FAS, which is not inhibited by triclosan [9].
  • In direct contrast to the delayed-death phenotype associated with poisoning of the apicoplast using certain other drugs, the rapid and striking action of triclosan suggests the possibility of developing new drug(s) for the treatment of malaria [9].
  • Triclosan that is used as an antibacterial agent against fatty acid synthesis type II 2-enoyl thioester reductases inhibited growth of FabI overexpressing mutant yeast cells but was not able to inhibit respiratory growth of the ETR2- or ETR1-complemented mutant yeast cells [10].

Chemical compound and disease context of triclosan


Biological context of triclosan

  • These data show that the formation of a noncovalent "bi-substrate" complex accounts for the effectiveness of triclosan as a FabI inhibitor and illustrates that mutations in the FabI active site that interfere with the formation of a stable FabI-NAD+-triclosan ternary complex acquire resistance to the drug [16].
  • Both the introduction of a plasmid expressing the safabI gene or a missense mutation in the chromosomal safabI gene led to triclosan resistance in S. aureus; however, these strains did not exhibit cross-resistance to hexachlorophene [11].
  • Molecular genetic studies with strains of Escherichia coli resistant to triclosan, an ingredient of many anti-bacterial household goods, have suggested that this compound works by acting as an inhibitor of enoyl reductase (ENR) and thereby blocking lipid biosynthesis [17].
  • Antibacterial product use did not lead to a significant increase in antimicrobial drug resistance after 1 year (odds ratio 1.33, 95% confidence interval 0.74-2.41), nor did it have an effect on bacterial susceptibility to triclosan [18].
  • The compounds exploit beta-lactamases to release triclosan through hydrolysis of the beta-lactam ring [19].

Anatomical context of triclosan

  • These data provide a molecular mechanism for the antibacterial activity of triclosan and substantiate the hypothesis that its activity results from inhibition of a specific cellular target rather than non-specific disruption of the bacterial cell membrane [20].
  • Effect of triclosan on the development of bacterial biofilms by urinary tract pathogens on urinary catheters [21].
  • This suggests that, in C. gingivalis, TMP may diffuse into the cell wall more easily than triclosan and then be converted to triclosan by phosphatase activity within the cell wall complex, where it may give rise to high localized concentrations and subsequent cell damage [22].
  • Previously, we reported that triclosan reduces the production of the inflammatory mediators in gingival fibroblasts [23].
  • This very low solubility can hamper its biological activity in the oral cavity, which could explain the mixed clinical results obtained from triclosan toothpaste trials [24].

Associations of triclosan with other chemical compounds

  • Although all three compounds inhibit mycolic acid synthesis, treatment with INH and TLM, but not with TRC, results in the accumulation of ACP-bound lipid precursors to mycolic acids that were 26 carbons long and fully saturated [3].
  • Specific inhibitors of the type II pathway, thiolactomycin and triclosan, have been reported to target this Plasmodium pathway [25].
  • Following hydrolysis of possible conjugates, triclosan is extracted with n-hexane/acetone, partitioned into alcoholic potassium hydroxide, and converted into its pentafluorobenzoyl ester [26].
  • We present here the results for one of the beta-lactamase ECTA compounds, NB2001, which consists of the antibacterial agent triclosan in a prodrug form with a cephalosporin scaffold [27].
  • The site of action of isoniazid, used in the treatment of tuberculosis for 50 years, and the consumer antimicrobial agent triclosan were revealed recently to be the enoyl-ACP reductase of the type II FAS [28].

Gene context of triclosan

  • (i) NB2001 is a substrate for TEM-1 beta-lactamase, forming triclosan with a second-order rate constant (k(cat)/K(m)) of greater than 77,000 M-1 s-1 [27].
  • Studies of 3-OH-BaP sulfonation by expressed human SULT1A1*1, SULT1A1*2, SULT1B1, and SULT1E1 showed that triclosan inhibited the activities of each of these purified enzymes with IC50 concentrations between 2.09 and 7.5 microM [29].
  • The pesticide trans-nonachlor activation was 53.8%, while the widely used bacteriocide triclosan was a medium activator of hPXR at 46.2% [30].
  • Moreover, enhanced COX-2 mRNA repression was observed with triclosan and CPC in comparison to triclosan alone in IL-1beta and TNF-alpha stimulated cells [31].
  • Further analysis of cell signaling mechanisms of triclosan and CPC indicates that nuclear factor-kappa B (NF-kappaB) and not p38 mitogen-activated protein kinase (MAPK) signaling may be impaired in the presence of triclosan and CPC [31].

Analytical, diagnostic and therapeutic context of triclosan

  • These results indicate that triclosan suppresses rat mammary carcinogenesis by inhibiting FAS and suggest that FAS is a promising molecular target for breast cancer chemoprevention [32].
  • Gel filtration and mass spectrometry show that inhibition by triclosan is reversible [33].
  • Similarly 9 of 13 triclosan eluting stents showed no viable organisms upon recovery and the remaining 4 showed significantly fewer organisms than controls [34].
  • HPLC was used to determine the triclosan concentration in urine draining from models that had been fitted with triclosan-inflated silicone catheters [21].
  • Uncured MDPB revealed antibacterial activity against S. mutans and six other species of oral streptococci, with the minimum inhibitory concentration for S. mutans being comparable with that of triclosan [35].


  1. Triclosan-resistant Staphylococcus aureus. Uhl, S. Lancet (1993) [Pubmed]
  2. The enoyl-[acyl-carrier-protein] reductases FabI and FabL from Bacillus subtilis. Heath, R.J., Su, N., Murphy, C.K., Rock, C.O. J. Biol. Chem. (2000) [Pubmed]
  3. Isoniazid affects multiple components of the type II fatty acid synthase system of Mycobacterium tuberculosis. Slayden, R.A., Lee, R.E., Barry, C.E. Mol. Microbiol. (2000) [Pubmed]
  4. Topical triclosan treatment of atopic dermatitis. Sporik, R., Kemp, A.S. J. Allergy Clin. Immunol. (1997) [Pubmed]
  5. Effects of triclosan-containing rinse on the dynamics and antimicrobial susceptibility of in vitro plaque ecosystems. McBain, A.J., Bartolo, R.G., Catrenich, C.E., Charbonneau, D., Ledder, R.G., Gilbert, P. Antimicrob. Agents Chemother. (2003) [Pubmed]
  6. Antimicrobial effects of a new therapeutic liquid dentifrice formulation on oral bacteria including odorigenic species. Sreenivasan, P.K., Furgang, D., Zhang, Y., DeVizio, W., Fine, D.H. Clinical oral investigations. (2005) [Pubmed]
  7. Triclosan offers protection against blood stages of malaria by inhibiting enoyl-ACP reductase of Plasmodium falciparum. Surolia, N., Surolia, A. Nat. Med. (2001) [Pubmed]
  8. Transferable resistance to triclosan in MRSA. Cookson, B.D., Farrelly, H., Stapleton, P., Garvey, R.P., Price, M.R. Lancet (1991) [Pubmed]
  9. Paradigm shifts in malaria parasite biochemistry and anti-malarial chemotherapy. Surolia, N., RamachandraRao, S.P., Surolia, A. Bioessays (2002) [Pubmed]
  10. Candida tropicalis expresses two mitochondrial 2-enoyl thioester reductases that are able to form both homodimers and heterodimers. Torkko, J.M., Koivuranta, K.T., Kastaniotis, A.J., Airenne, T.T., Glumoff, T., Ilves, M., Hartig, A., Gurvitz, A., Hiltunen, J.K. J. Biol. Chem. (2003) [Pubmed]
  11. Inhibition of the Staphylococcus aureus NADPH-dependent enoyl-acyl carrier protein reductase by triclosan and hexachlorophene. Heath, R.J., Li, J., Roland, G.E., Rock, C.O. J. Biol. Chem. (2000) [Pubmed]
  12. N-alpha-Cocoyl-L-arginine ethyl ester, DL-pyroglutamic acid salt, as an inactivator of hepatitis B surface antigen. Sugimoto, Y., Toyoshima, S. Antimicrob. Agents Chemother. (1979) [Pubmed]
  13. The effect of triclosan toothpaste on enamel demineralization in a bacterial demineralization model. van Loveren, C., Buijs, J.F., ten Cate, J.M. J. Antimicrob. Chemother. (2000) [Pubmed]
  14. Agents for the management of plaque and gingivitis. Ciancio, S.G. J. Dent. Res. (1992) [Pubmed]
  15. The MexJK efflux pump of Pseudomonas aeruginosa requires OprM for antibiotic efflux but not for efflux of triclosan. Chuanchuen, R., Narasaki, C.T., Schweizer, H.P. J. Bacteriol. (2002) [Pubmed]
  16. Mechanism of triclosan inhibition of bacterial fatty acid synthesis. Heath, R.J., Rubin, J.R., Holland, D.R., Zhang, E., Snow, M.E., Rock, C.O. J. Biol. Chem. (1999) [Pubmed]
  17. Crystallographic analysis of triclosan bound to enoyl reductase. Roujeinikova, A., Levy, C.W., Rowsell, S., Sedelnikova, S., Baker, P.J., Minshull, C.A., Mistry, A., Colls, J.G., Camble, R., Stuitje, A.R., Slabas, A.R., Rafferty, J.B., Pauptit, R.A., Viner, R., Rice, D.W. J. Mol. Biol. (1999) [Pubmed]
  18. Antibacterial cleaning products and drug resistance. Aiello, A.E., Marshall, B., Levy, S.B., Della-Latta, P., Lin, S.X., Larson, E. Emerging Infect. Dis. (2005) [Pubmed]
  19. Mechanism of action of NB2001 and NB2030, novel antibacterial agents activated by beta-lactamases. Stone, G.W., Zhang, Q., Castillo, R., Doppalapudi, V.R., Bueno, A.R., Lee, J.Y., Li, Q., Sergeeva, M., Khambatta, G., Georgopapadakou, N.H. Antimicrob. Agents Chemother. (2004) [Pubmed]
  20. Structural basis and mechanism of enoyl reductase inhibition by triclosan. Stewart, M.J., Parikh, S., Xiao, G., Tonge, P.J., Kisker, C. J. Mol. Biol. (1999) [Pubmed]
  21. Effect of triclosan on the development of bacterial biofilms by urinary tract pathogens on urinary catheters. Jones, G.L., Muller, C.T., O'Reilly, M., Stickler, D.J. J. Antimicrob. Chemother. (2006) [Pubmed]
  22. Effects of triclosan and triclosan monophosphate on maximum specific growth rates, biomass and hydrolytic enzyme production of Streptococcus sanguis and Capnocytophaga gingivalis in continuous culture. Greenman, J., McKenzie, C., Nelson, D.G. J. Antimicrob. Chemother. (1997) [Pubmed]
  23. Uptake, distribution and release of 14C-triclosan in human gingival fibroblasts. Mustafa, M., Wondimu, B., Hultenby, K., Yucel-Lindberg, T., Modéer, T. Journal of pharmaceutical sciences. (2003) [Pubmed]
  24. Effect of cyclodextrins and polymers on triclosan availability and substantivity in toothpastes in vivo. Loftsson, T., Leeves, N., Bjornsdottir, B., Duffy, L., Masson, M. Journal of pharmaceutical sciences. (1999) [Pubmed]
  25. A type II pathway for fatty acid biosynthesis presents drug targets in Plasmodium falciparum. Waller, R.F., Ralph, S.A., Reed, M.B., Su, V., Douglas, J.D., Minnikin, D.E., Cowman, A.F., Besra, G.S., McFadden, G.I. Antimicrob. Agents Chemother. (2003) [Pubmed]
  26. Determination of triclosan as its pentafluorobenzoyl ester in human plasma and milk using electron capture negative ionization mass spectrometry. Allmyr, M., McLachlan, M.S., Sandborgh-Englund, G., Adolfsson-Erici, M. Anal. Chem. (2006) [Pubmed]
  27. NB2001, a novel antibacterial agent with broad-spectrum activity and enhanced potency against beta-lactamase-producing strains. Li, Q., Lee, J.Y., Castillo, R., Hixon, M.S., Pujol, C., Doppalapudi, V.R., Shepard, H.M., Wahl, G.M., Lobl, T.J., Chan, M.F. Antimicrob. Agents Chemother. (2002) [Pubmed]
  28. Lipid biosynthesis as a target for antibacterial agents. Heath, R.J., White, S.W., Rock, C.O. Prog. Lipid Res. (2001) [Pubmed]
  29. Triclosan as a substrate and inhibitor of 3'-phosphoadenosine 5'-phosphosulfate-sulfotransferase and UDP-glucuronosyl transferase in human liver fractions. Wang, L.Q., Falany, C.N., James, M.O. Drug Metab. Dispos. (2004) [Pubmed]
  30. Lignans, bacteriocides and organochlorine compounds activate the human pregnane X receptor (PXR). Jacobs, M.N., Nolan, G.T., Hood, S.R. Toxicol. Appl. Pharmacol. (2005) [Pubmed]
  31. Prostaglandin production by human gingival fibroblasts inhibited by triclosan in the presence of cetylpyridinium chloride. Kim, Y.J., Rossa, C., Kirkwood, K.L. J. Periodontol. (2005) [Pubmed]
  32. Fatty acid synthase is a potential molecular target for the chemoprevention of breast cancer. Lu, S., Archer, M.C. Carcinogenesis (2005) [Pubmed]
  33. Kinetic and structural characteristics of the inhibition of enoyl (acyl carrier protein) reductase by triclosan. Ward, W.H., Holdgate, G.A., Rowsell, S., McLean, E.G., Pauptit, R.A., Clayton, E., Nichols, W.W., Colls, J.G., Minshull, C.A., Jude, D.A., Mistry, A., Timms, D., Camble, R., Hales, N.J., Britton, C.J., Taylor, I.W. Biochemistry (1999) [Pubmed]
  34. Triclosan loaded ureteral stents decrease proteus mirabilis 296 infection in a rabbit urinary tract infection model. Cadieux, P.A., Chew, B.H., Knudsen, B.E., Dejong, K., Rowe, E., Reid, G., Denstedt, J.D. J. Urol. (2006) [Pubmed]
  35. Incorporation of bacterial inhibitor into resin composite. Imazato, S., Torii, M., Tsuchitani, Y., McCabe, J.F., Russell, R.R. J. Dent. Res. (1994) [Pubmed]
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