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Chemical Compound Review

CPD-4506     10-[3-(4-methylpyrazin-1- yl)propyl]-2...

Synonyms: AC1L9H2I
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Disease relevance of trifluoperazine


High impact information on trifluoperazine

  • The potential antiarrhythmic and electrophysiological actions of drugs known to inhibit calmodulin, i.e. trifluoperazine (TFP) and N-(6-aminohexyl)-5-chloro-1-naphthalene sulphonamide (W7) have been compared with bepridil, whose antiarrhythmic actions have previously been ascribed to blockade of the fast inward sodium current in cardiac tissue [1].
  • The effect of regucalcin (10(-7) M) in decreasing NO synthase activity was also seen in the presence of TFP (50 microM) or EGTA (1 mM) [2].
  • The biological implications from the cooperative, non-specific interaction of CPZ and TFP with membranes are also commented upon [4].
  • Phenothiazine derivatives chlorpromazine (cpz) and trifluoperazine (tfp) were found to induce apoptosis, abnormal cell cycle and expression of p53 in Chinese hamster lung fibroblast V79 cells [5].
  • Since it is known that the inhibitory effect of TFP or CHP against calmodulin-dependent enzymes such as phosphodiesterase is 100-400-fold higher compared to PMZ, it is speculated that the inhibitory effect of TFP or CHP against cyanide-induced convulsions may be based on its strong inhibitory properties into calmodulin-dependent enzymes [6].

Chemical compound and disease context of trifluoperazine

  • Although TFP was shown to possess alpha-adrenoceptor blocking properties, the classical alpha-blocker, phentolamine, failed to reduce significantly the incidence or severity of reperfusion arrhythmias [1].

Biological context of trifluoperazine

  • On the other hand, the LD50 value of cyanide was significantly increased by i.v.t. preadministration of TFP or CHP (0.045 mumol/body) [6].

Anatomical context of trifluoperazine

  • These effects of calmodulin and TFP are consistent with the notion of a plasma membrane origin for this activity and also suggest that this activity could be a basis for the regulation of intracellular Ca2+ activity in the submicromolar range [7].
  • The Ca2+ effect was significantly inhibited by trifluoperazine (TFP; 20 or 50 microM), an antagonist of calmodulin, indicating the existence of Ca2+/calmodulin-dependent NO synthase activity in rat heart muscle cytosol [8].
  • Experiments using vesicles prepared from brush-border or basolateral membranes indicated that TFP inhibited the calcium-extrusion process, with virtually no effect on calcium entry [9].

Gene context of trifluoperazine

  • Regucalcin significantly reduced NO synthase activity in the presence of TFP (50 micro micro M) or EGTA (1 mM) which has a significant inhibitory effect on the enzyme activity [10].


  1. Comparative antiarrhythmic and electrophysiological effects of drugs known to inhibit calmodulin (TFP, W7 and bepridil). Barron, E., Marshall, R.J., Martorana, M., Winslow, E. Br. J. Pharmacol. (1986) [Pubmed]
  2. Suppressive effect of endogenous regucalcin on nitric oxide synthase activity in cloned rat hepatoma H4-II-E cells overexpressing regucalcin. Izumi, T., Tsurusaki, Y., Yamaguchi, M. J. Cell. Biochem. (2003) [Pubmed]
  3. Synergistic induction of apoptosis in breast cancer cells by tamoxifen and calmodulin inhibitors. Frankfurt, O.S., Sugarbaker, E.V., Robb, J.A., Villa, L. Cancer Lett. (1995) [Pubmed]
  4. Interaction of two phenothiazine derivatives with phospholipid monolayers. Hidalgo, A.A., Caetano, W., Tabak, M., Oliveira, O.N. Biophys. Chem. (2004) [Pubmed]
  5. Induction of apoptosis by Phenothiazine derivatives in V79 cells. Karmakar, P., Natarajan, A.T., Poddar, R.K., Dasgupta, U.B. Toxicol. Lett. (2001) [Pubmed]
  6. Protective effect of calmodulin inhibitors against acute cyanide-induced lethality and convulsions in mice. Yamamoto, H. Toxicol. Lett. (1993) [Pubmed]
  7. Ca-stimulated Mg dependent ATPase activity in a plasma membrane enriched fraction of bovine corneal epithelium. Reinach, P., Holmberg, N. Curr. Eye Res. (1987) [Pubmed]
  8. Suppressive role of endogenous regucalcin in the regulation of nitric oxide synthase activity in heart muscle cytosol of normal and regucalcin transgenic rats. Ma, Z.J., Yamaguchi, M. Int. J. Mol. Med. (2002) [Pubmed]
  9. Localization of vitamin D-dependent active Ca2+ transport in rat duodenum and relation to CaBP. Roche, C., Bellaton, C., Pansu, D., Miller, A., Bronner, F. Am. J. Physiol. (1986) [Pubmed]
  10. Regulatory effect of regucalcin on nitric oxide synthase activity in rat kidney cortex cytosol: Role of endogenous regucalcin in transgenic rats. Ma, Z.J., Yamaguchi, M. Int. J. Mol. Med. (2003) [Pubmed]
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