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Chemical Compound Review

Lopac-N-170     3-[2-hydroxy-5- (trifluoromethyl)phenyl]-6...

Synonyms: CHEMBL384903, N170_SIGMA, AG-J-69525, BSPBio_001425, KBioGR_000145, ...
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Disease relevance of Lopac-N-170

  • In the current study, we examined pial arteriolar responses to forskolin, dibutyryl-cAMP, NS-1619, and methionine (met)-enkephalin, activators of calcium-dependent K+ channels (K(Ca)) before and 1 hour after 10 minutes of total, global ischemia in anesthetized piglets [1].
  • Additionally, we show that BK and NS-1619 significantly increased the density of transport vesicles in the cytoplasm of brain tumor capillary endothelia and tumor cells [2].

High impact information on Lopac-N-170

  • ANG II (10 nM) decreased afferent arteriolar diameter by 44 +/- 4%, a response that was reduced by 30% during NS-1619 treatment; however, TEA failed to alter afferent constrictor responses to either ANG II or arginine vasopressin [3].
  • 1. The effects of intracellular redox couples were investigated on the activation by voltage, Ca2+ and NS 1619 of maxi-K channels in enzymatically isolated smooth muscle cells from large pulmonary arteries of rabbits [4].
  • NS 1619 also predisposed the maxi-K channel to open at more hyperpolarized membrane potentials [4].
  • To test this hypothesis, we measured effects of NS-1619, a putative mtK(Ca) channel opener, and valinomycin, a K(+) ionophore, on mitochondrial respiration, DeltaPsi(m), and ROS generation in guinea pig heart mitochondria [5].
  • Voltage-clamp recordings indicated that IBTX-sensitive currents were not enhanced to the extent observed in nondiabetic controls by increasing the Ca(2+) concentration in the pipette solution or the application of NS-1619 in myocytes from diabetic animals [6].

Biological context of Lopac-N-170


Anatomical context of Lopac-N-170

  • 8. NS 1619 (3-100 microM) produced a concentration-dependent inhibition of spontaneous activity in rat portal vein characterized by a reduction in the amplitude and duration of the tension waves [10].
  • BK channel activation by NS-1619 is partially mediated by intracellular Ca2+ release in smooth muscle cells of porcine coronary artery [11].
  • Activation of BKCa channels in acutely dissociated neurones from the rat ventromedial hypothalamus by NS 1619 [12].
  • Ion channel modulation by NS 1619, the putative BKCa channel opener, in vascular smooth muscle [10].
  • NS-1619 (a Ca(2+)-sensitive K(+) activator) elicited heightened effects in the aortas of pregnant animals receiving 0.9% NaCl supplementation [13].

Associations of Lopac-N-170 with other chemical compounds

  • In contrast, coadministration of exogenous HSP-70 (1 mug/ml) potentiated dilation to cromakalim, CGRP, and NS-1619 [14].
  • Unlike diazoxide (the opener of mitochondrial KATP channels), NS-1619 did not increase the expression of inducible or endothelial NOS [15].
  • Cumulative concentration-response curves to low-affinity state beta1-AR agonists (CGP 12177, cyanopindolol or alprenolol) and to NS 1619, a large conductance Ca2+-activated K+ channels (BK) agonist were performed in denuded aortic rings isolated from control or treated Wistar Kyoto (WKY) rats or SHRs in different experimental conditions [16].
  • NS 1619 reduced electrically stimulated contractile responses of rat vas deferens in a concentration-dependent manner, and charybdotoxin but not glibenclamide partially inhibited the effect of NS 1619 [17].
  • The K(Ca) channel openers NS 1619 and 1-EBIO elicit relaxation effects that are not diminished after removal of the endothelium and are not inhibited by ouabain/Ba2+ [18].

Gene context of Lopac-N-170

  • Under nonbrain injury conditions, topical coadministration of exogenous HSP-27 (1 mug/ml) blunted dilation to cromakalim, CGRP, and NS-1619 (10(-8) and 10(-6) M; cromakalim and CGRP are K(ATP) agonists and NS-1619 is a K(Ca) agonist) [14].
  • This infarct-limiting effect of NS-1619 was associated with improvement in ventricular functional recovery after I/R [15].
  • Furthermore, activation of BK(Ca) channels with NS-1619 was three times more effective at increasing outward current in cells from control versus IR animals [19].
  • The effect of NS 1619 on the BK channel was dose-dependent, resulting in a shift of the activation curve by up to -50 mV towards negative membrane potentials [20].
  • NS-1619, another BK channel opener, induced gradual but substantial change in F/F(K) even in native HEK, while the BK channel opening effect was detected [21].

Analytical, diagnostic and therapeutic context of Lopac-N-170

  • Finally, whole-cell recordings of outward K(+) current detected a prominent iberiotoxin-sensitive BK(Ca) current in SMCs that was absent in ECs, and the BK(Ca) channel opener NS 1619 only enhanced K(+) current in the SMCs [22].
  • Neither NS-1619 nor TEA altered agonist-induced constriction of the efferent arteriole [3].
  • Adult male ICR mice were pretreated with the KCa-channel opener NS-1619 either 10 min or 24 h before 30 min of global ischemia and 60 min of reperfusion (I/R) in Langendorff mode [15].
  • We were able to biochemically modulate one such protein marker, the calcium-dependent potassium (K(Ca)) channel, by using a specific K(Ca) channel agonist, NS-1619, to obtain sustained enhancement of selective drug delivery, including molecules of varying sizes, to tumors in rat syngeneic and xenograft brain tumor models [23].


  1. Calcium-activated K+ channels in cerebral arterioles in piglets are resistant to ischemia. Bari, F., Louis, T.M., Busija, D.W. J. Cereb. Blood Flow Metab. (1997) [Pubmed]
  2. Regulation of blood-brain tumor barrier permeability by calcium-activated potassium channels. Ningaraj, N.S., Rao, M., Hashizume, K., Asotra, K., Black, K.L. J. Pharmacol. Exp. Ther. (2002) [Pubmed]
  3. Influence of Ca(2+)-activated K(+) channels on rat renal arteriolar responses to depolarizing agonists. Fallet, R.W., Bast, J.P., Fujiwara, K., Ishii, N., Sansom, S.C., Carmines, P.K. Am. J. Physiol. Renal Physiol. (2001) [Pubmed]
  4. Contrasting effects of intracellular redox couples on the regulation of maxi-K channels in isolated myocytes from rabbit pulmonary artery. Thuringer, D., Findlay, I. J. Physiol. (Lond.) (1997) [Pubmed]
  5. Mitochondrial Ca2+-induced K+ influx increases respiration and enhances ROS production while maintaining membrane potential. Heinen, A., Camara, A.K., Aldakkak, M., Rhodes, S.S., Riess, M.L., Stowe, D.F. Am. J. Physiol., Cell Physiol. (2007) [Pubmed]
  6. Reduced Ca2+-dependent activation of large-conductance Ca2+-activated K+ channels from arteries of Type 2 diabetic Zucker diabetic fatty rats. Burnham, M.P., Johnson, I.T., Weston, A.H. Am. J. Physiol. Heart Circ. Physiol. (2006) [Pubmed]
  7. Inhibition of guinea pig detrusor contraction by NS-1619 is associated with activation of BKCa and inhibition of calcium currents. Sheldon, J.H., Norton, N.W., Argentieri, T.M. J. Pharmacol. Exp. Ther. (1997) [Pubmed]
  8. Role of nucleotide cyclases in the inhibition of pregnant rat uterine contractions by the openers of potassium channels. Okawa, T., Longo, M., Vedernikov, Y.P., Chwalisz, K., Saade, G.R., Garfield, R.E. Am. J. Obstet. Gynecol. (2000) [Pubmed]
  9. Melatonin directly constricts rat cerebral arteries through modulation of potassium channels. Geary, G.G., Krause, D.N., Duckles, S.P. Am. J. Physiol. (1997) [Pubmed]
  10. Ion channel modulation by NS 1619, the putative BKCa channel opener, in vascular smooth muscle. Edwards, G., Niederste-Hollenberg, A., Schneider, J., Noack, T., Weston, A.H. Br. J. Pharmacol. (1994) [Pubmed]
  11. BK channel activation by NS-1619 is partially mediated by intracellular Ca2+ release in smooth muscle cells of porcine coronary artery. Yamamura, H., Ohi, Y., Muraki, K., Watanabe, M., Imaizumi, Y. Br. J. Pharmacol. (2001) [Pubmed]
  12. Activation of BKCa channels in acutely dissociated neurones from the rat ventromedial hypothalamus by NS 1619. Sellers, A.J., Ashford, M.L. Br. J. Pharmacol. (1994) [Pubmed]
  13. Increased Na+ intake during gestation in rats is associated with enhanced vascular reactivity and alterations of K+ and Ca2+ function. Auger, K., Beauséjour, A., Brochu, M., St-Louis, J. Am. J. Physiol. Heart Circ. Physiol. (2004) [Pubmed]
  14. Heat shock protein modulation of KATP and KCa channel cerebrovasodilation after brain injury. Armstead, W.M., Hecker, J.G. Am. J. Physiol. Heart Circ. Physiol. (2005) [Pubmed]
  15. Opening of Ca2+-activated K+ channels triggers early and delayed preconditioning against I/R injury independent of NOS in mice. Wang, X., Yin, C., Xi, L., Kukreja, R.C. Am. J. Physiol. Heart Circ. Physiol. (2004) [Pubmed]
  16. Low-affinity state beta1-adrenoceptor-induced vasodilation in SHR. Mallem, M.Y., Reculeau, O., Le Coz, O., Gogny, M., Desfontis, J.C. Peptides (2005) [Pubmed]
  17. NS 1619 activates Ca2+-activated K+ currents in rat vas deferens. Huang, Y., Lau, C.W., Ho, I.H. Eur. J. Pharmacol. (1997) [Pubmed]
  18. EDHF-mediated relaxation in rat gastric small arteries: influence of ouabain/Ba2+ and relation to potassium ions. Van de Voorde, J., Vanheel, B. J. Cardiovasc. Pharmacol. (2000) [Pubmed]
  19. Potassium (BK(Ca)) currents are reduced in microvascular smooth muscle cells from insulin-resistant rats. Dimitropoulou, C., Han, G., Miller, A.W., Molero, M., Fuchs, L.C., White, R.E., Carrier, G.O. Am. J. Physiol. Heart Circ. Physiol. (2002) [Pubmed]
  20. Selective activation of Ca(2+)-dependent K+ channels by novel benzimidazolone. Olesen, S.P., Munch, E., Moldt, P., Drejer, J. Eur. J. Pharmacol. (1994) [Pubmed]
  21. Usefulness and limitation of DiBAC4(3), a voltage-sensitive fluorescent dye, for the measurement of membrane potentials regulated by recombinant large conductance Ca2+-activated K+ channels in HEK293 cells. Yamada, A., Gaja, N., Ohya, S., Muraki, K., Narita, H., Ohwada, T., Imaizumi, Y. Jpn. J. Pharmacol. (2001) [Pubmed]
  22. Freshly isolated bovine coronary endothelial cells do not express the BK Ca channel gene. Gauthier, K.M., Liu, C., Popovic, A., Albarwani, S., Rusch, N.J. J. Physiol. (Lond.) (2002) [Pubmed]
  23. Calcium-dependent potassium channels as a target protein for modulation of the blood-brain tumor barrier. Ningaraj, N.S., Rao, M., Black, K.L. Drug News Perspect. (2003) [Pubmed]
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