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Chemical Compound Review

SureCN1165652     4-(1-aminoethyl)-N-pyridin-4- yl...

Synonyms: SureCN1554110, Y0503_SIGMA, AC1L3XFM, LS-173023, EU-0100333, ...
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Disease relevance of 4-(1-aminoethyl)-N-pyridin-4-yl-cyclohexane-1-carboxamide


Psychiatry related information on 4-(1-aminoethyl)-N-pyridin-4-yl-cyclohexane-1-carboxamide


High impact information on 4-(1-aminoethyl)-N-pyridin-4-yl-cyclohexane-1-carboxamide

  • Using pharmacologic antagonism (Y-27632, ref. 13, 18), we examined the role of Rho-kinase in cavernosal tone, based on the hypothesis that antagonism of Rho-kinase results in increased corpus cavernosum pressure, initiating the erectile response independently of nitric oxide [8].
  • Here we show that a pyridine derivative, Y-27632, selectively inhibits smooth-muscle contraction by inhibiting Ca2+ sensitization [1].
  • Overexpression of LIM-kinase in HeLa cells induced the formation of actin stress fibers in a Y-27632-sensitive manner [9].
  • This phosphorylation was sensitive to Y-27632, a specific inhibitor of the Rho-associated kinase ROCK [9].
  • The hemodynamic effect of the Rho-kinase inhibitor (R)-(+)-trans-N-(4-pyridyl)-4-(1-aminoethyl)-cyclohexanecarboxamide (Y-27632) was determined in vivo by measuring changes in mean arterial pressure and systemic vascular resistance (SVR) (microspheres) [10].

Chemical compound and disease context of 4-(1-aminoethyl)-N-pyridin-4-yl-cyclohexane-1-carboxamide

  • Similarly, calcium mobilization is Galpha(q)-mediated and independent of Galpha(i/o) and Galpha(12/13) because pertussis toxin Y-27632 and had no effect, whereas U-73122 inhibition of phospholipase C-beta blocked the response [11].
  • Ten percent cyclic deformational strain (serum-free conditions) increased F-actin staining (152% over control), and this effect was enhanced by serum or lysophosphatidic acid (180%), but decreased (68%) with Clostridium botulinum toxin inhibition of RhoA or with the Rho kinase inhibitor Y27632 (67%) [12].
  • The aim of the present study was to test the hypothesis that an inhibitor specific for p160ROCK (Y27632) could prevent experimental hepatic fibrosis induced by dimethylnitrosamine (DMN) in rats [13].
  • Both the Rho kinase inhibitor Y27632 and the RhoA inhibitor toxin B (from Clostridium difficile) mimicked the statins' effects, enhancing doxorubicin accumulation, NO synthesis and IKKalpha phosphorylation and decreasing the amount of IkBalpha in HMM cells [14].
  • Since Y-27632 and fasudil depressed the contractions, it seems plausible to postulate that Rho-kinase inhibitors may be beneficial in the treatment of renal colic [15].

Biological context of 4-(1-aminoethyl)-N-pyridin-4-yl-cyclohexane-1-carboxamide

  • A specific inhibitor of Rho kinase, Y-27632, was used to examine the role of Rho kinase in inflammatory response in vivo and in vitro by molecular biology and by immunological and biochemical approaches [16].
  • CONCLUSIONS: Y27632 inhibited neointima formation by enhancing SMC apoptosis and probably by suppressing early SMC migration [17].
  • A specific ROCK inhibitor, Y27632, strongly suppressed MLC phosphorylation, cell motility, and invasion [18].
  • In parallel, dominant-negative RhoA (N19RhoA) and Y27632, a specific inhibitor of Rho-associated kinase, dramatically reverse the rounded cell morphology to a spread cell shape and enhance motility [19].
  • In addition, specific antisense oligonucleotides significantly diminished Rho kinase mRNA levels and replicated many of the teratologies induced by Y27632 [20].

Anatomical context of 4-(1-aminoethyl)-N-pyridin-4-yl-cyclohexane-1-carboxamide


Associations of 4-(1-aminoethyl)-N-pyridin-4-yl-cyclohexane-1-carboxamide with other chemical compounds

  • In addition, the p160ROCK-specific inhibitor Y-27632 inhibited increases in NHE1 activity in response to RhoA, and to lysophosphatidic acid (LPA), which stimulates RhoA, and it also inhibited LPA-increased phosphorylation of NHE1 [25].
  • Phenylephrine (PE)- and angiotensin 2 (AT2)-induced MAP increases were blunted in SMAKO mice, whereas the Rho-kinase inhibitor Y-27632 reduced MAP to the same extent in control and SMAKO mice [26].
  • In addition, HA1077 and Y-27632 inhibited 20-kD MLC phosphorylation at Ser19 and ATP secretion of platelets stimulated with STA2, thrombin (0.05 U/mL), and simultaneous addition of serotonin and epinephrine, whereas these compounds did not affect MLC phosphorylation or ATP secretion when platelets were stimulated with more than 0.1 U/mL thrombin [27].
  • Actin staining of S1P stimulated U118 cells overexpressing beta-galactosidase resulted in pronounced stress fiber formation that was exacerbated by S1P2 overexpression, partially blocked by S1P1, or totally abolished by pretreatment with Y-27632 [28].
  • In contrast, although RhoA T19N and Y-27632 blocked the cytoskeletal events induced by histamine, they had no effect on the stimulation of occludin phosphorylation or increased tracer flux, indicating that occludin phosphorylation may regulate tight junction permeability independently of cytoskeletal events [29].

Gene context of 4-(1-aminoethyl)-N-pyridin-4-yl-cyclohexane-1-carboxamide

  • We show that pharmacological inhibition of ROCK signaling by Y27632 resulted in increased glycosaminoglycan synthesis and elevated expression of the chondrogenic transcription factor Sox9, whereas overexpression of RhoA in the chondrogenic cell line ATDC5 had the opposite effects [30].
  • In contrast, neither ERK1/2 nor p38 phosphorylation was abrogated by Y-27632 [31].
  • Moreover, treatment of cells with RhoA-dependent protein kinase (p160-ROCK) inhibitor Y27632 yielded cytoskeletal organization similar to that of CB2-stimulated cells [32].
  • In addition, Y27632 reversed the cell morphology and abolished the contractility of TGF-beta-treated cells [33].
  • Furthermore, the expression of a dominant negative mutant of Ect2, a Rho GEF, or Y-27632, an inhibitor of the Rho-dependent kinase ROCK, inhibited cytokinesis in HeLa cells but not in Rat1A cells [34].

Analytical, diagnostic and therapeutic context of 4-(1-aminoethyl)-N-pyridin-4-yl-cyclohexane-1-carboxamide

  • Oral administration of Y-27632 in rats significantly reduced the colonic inflammation [16].
  • In vitro studies with prototypical ROCK inhibitors such as Y27632 and in vivo data from animal models indicate that such drugs have potential as future treatments for bladder dysfunction [35].
  • Y27632 significantly increased the neointimal TUNEL(+) SMCs at days 7 and 14, but not BrdU(+) SMCs [17].
  • The primary tumor volume at the site of injection was smaller in the Y-27632-treated group compared with the control group, but the difference was not statistically significant [5].
  • Y-27632 reduced the basal perfusion pressure of in situ perfused livers in BDL rats but not in sham operated rats [36].


  1. Calcium sensitization of smooth muscle mediated by a Rho-associated protein kinase in hypertension. Uehata, M., Ishizaki, T., Satoh, H., Ono, T., Kawahara, T., Morishita, T., Tamakawa, H., Yamagami, K., Inui, J., Maekawa, M., Narumiya, S. Nature (1997) [Pubmed]
  2. Activation of G12/G13 results in shape change and Rho/Rho-kinase-mediated myosin light chain phosphorylation in mouse platelets. Klages, B., Brandt, U., Simon, M.I., Schultz, G., Offermanns, S. J. Cell Biol. (1999) [Pubmed]
  3. Ephrin-A5 induces collapse of growth cones by activating Rho and Rho kinase. Wahl, S., Barth, H., Ciossek, T., Aktories, K., Mueller, B.K. J. Cell Biol. (2000) [Pubmed]
  4. Inhibition of Rho-kinase affects astrocytoma morphology, motility, and invasion through activation of Rac1. Salhia, B., Rutten, F., Nakada, M., Beaudry, C., Berens, M., Kwan, A., Rutka, J.T. Cancer Res. (2005) [Pubmed]
  5. Inhibition of intrahepatic metastasis of human hepatocellular carcinoma by Rho-associated protein kinase inhibitor Y-27632. Takamura, M., Sakamoto, M., Genda, T., Ichida, T., Asakura, H., Hirohashi, S. Hepatology (2001) [Pubmed]
  6. Effect of doxazosin with and without rho-kinase inhibitor on human corpus cavernosum smooth muscle in the presence of bladder outlet obstruction. Demir, O., Murat, N., Aslan, G., Gidener, S., Esen, A.A. J. Urol. (2006) [Pubmed]
  7. Nonsteroidal anti-inflammatory drugs can lower amyloidogenic Abeta42 by inhibiting Rho. Zhou, Y., Su, Y., Li, B., Liu, F., Ryder, J.W., Wu, X., Gonzalez-DeWhitt, P.A., Gelfanova, V., Hale, J.E., May, P.C., Paul, S.M., Ni, B. Science (2003) [Pubmed]
  8. Antagonism of Rho-kinase stimulates rat penile erection via a nitric oxide-independent pathway. Chitaley, K., Wingard, C.J., Clinton Webb, R., Branam, H., Stopper, V.S., Lewis, R.W., Mills, T.M. Nat. Med. (2001) [Pubmed]
  9. Signaling from Rho to the actin cytoskeleton through protein kinases ROCK and LIM-kinase. Maekawa, M., Ishizaki, T., Boku, S., Watanabe, N., Fujita, A., Iwamatsu, A., Obinata, T., Ohashi, K., Mizuno, K., Narumiya, S. Science (1999) [Pubmed]
  10. Defective RhoA/Rho-kinase signaling contributes to vascular hypocontractility and vasodilation in cirrhotic rats. Hennenberg, M., Biecker, E., Trebicka, J., Jochem, K., Zhou, Q., Schmidt, M., Jakobs, K.H., Sauerbruch, T., Heller, J. Gastroenterology (2006) [Pubmed]
  11. Functional selectivity of G protein signaling by agonist peptides and thrombin for the protease-activated receptor-1. McLaughlin, J.N., Shen, L., Holinstat, M., Brooks, J.D., Dibenedetto, E., Hamm, H.E. J. Biol. Chem. (2005) [Pubmed]
  12. Mechanical stress increases RhoA activation in airway smooth muscle cells. Smith, P.G., Roy, C., Zhang, Y.N., Chauduri, S. Am. J. Respir. Cell Mol. Biol. (2003) [Pubmed]
  13. A selective ROCK inhibitor, Y27632, prevents dimethylnitrosamine-induced hepatic fibrosis in rats. Tada, S., Iwamoto, H., Nakamuta, M., Sugimoto, R., Enjoji, M., Nakashima, Y., Nawata, H. J. Hepatol. (2001) [Pubmed]
  14. Statins revert doxorubicin resistance via nitric oxide in malignant mesothelioma. Riganti, C., Orecchia, S., Pescarmona, G., Betta, P.G., Ghigo, D., Bosia, A. Int. J. Cancer (2006) [Pubmed]
  15. Expression of Rho-kinase (ROCK-1 and ROCK-2) and its substantial role in the contractile activity of the sheep ureter. Levent, A., Büyükafsar, K. Br. J. Pharmacol. (2004) [Pubmed]
  16. Rho kinase blockade prevents inflammation via nuclear factor kappa B inhibition: evidence in Crohn's disease and experimental colitis. Segain, J.P., Raingeard de la Blétière, D., Sauzeau, V., Bourreille, A., Hilaret, G., Cario-Toumaniantz, C., Pacaud, P., Galmiche, J.P., Loirand, G. Gastroenterology (2003) [Pubmed]
  17. Role of Rho-associated kinase in neointima formation after vascular injury. Shibata, R., Kai, H., Seki, Y., Kato, S., Morimatsu, M., Kaibuchi, K., Imaizumi, T. Circulation (2001) [Pubmed]
  18. E1AF/PEA3 activates the Rho/Rho-associated kinase pathway to increase the malignancy potential of non-small-cell lung cancer cells. Hakuma, N., Kinoshita, I., Shimizu, Y., Yamazaki, K., Yoshida, K., Nishimura, M., Dosaka-Akita, H. Cancer Res. (2005) [Pubmed]
  19. The COOH-terminal end of R-Ras alters the motility and morphology of breast epithelial cells through Rho/Rho-kinase. Jeong, H.W., Nam, J.O., Kim, I.S. Cancer Res. (2005) [Pubmed]
  20. Rho kinases play an obligatory role in vertebrate embryonic organogenesis. Wei, L., Roberts, W., Wang, L., Yamada, M., Zhang, S., Zhao, Z., Rivkees, S.A., Schwartz, R.J., Imanaka-Yoshida, K. Development (2001) [Pubmed]
  21. Rho kinase regulates tight junction function and is necessary for tight junction assembly in polarized intestinal epithelia. Walsh, S.V., Hopkins, A.M., Chen, J., Narumiya, S., Parkos, C.A., Nusrat, A. Gastroenterology (2001) [Pubmed]
  22. Molecular dissection of the Rho-associated protein kinase (p160ROCK)-regulated neurite remodeling in neuroblastoma N1E-115 cells. Hirose, M., Ishizaki, T., Watanabe, N., Uehata, M., Kranenburg, O., Moolenaar, W.H., Matsumura, F., Maekawa, M., Bito, H., Narumiya, S. J. Cell Biol. (1998) [Pubmed]
  23. Effects of cell tension on the small GTPase Rac. Katsumi, A., Milanini, J., Kiosses, W.B., del Pozo, M.A., Kaunas, R., Chien, S., Hahn, K.M., Schwartz, M.A. J. Cell Biol. (2002) [Pubmed]
  24. Cooperative effects of Rho and mechanical stretch on stress fiber organization. Kaunas, R., Nguyen, P., Usami, S., Chien, S. Proc. Natl. Acad. Sci. U.S.A. (2005) [Pubmed]
  25. p160ROCK mediates RhoA activation of Na-H exchange. Tominaga, T., Ishizaki, T., Narumiya, S., Barber, D.L. EMBO J. (1998) [Pubmed]
  26. Dominant role of smooth muscle L-type calcium channel Cav1.2 for blood pressure regulation. Moosmang, S., Schulla, V., Welling, A., Feil, R., Feil, S., Wegener, J.W., Hofmann, F., Klugbauer, N. EMBO J. (2003) [Pubmed]
  27. Agonist-induced regulation of myosin phosphatase activity in human platelets through activation of Rho-kinase. Suzuki, Y., Yamamoto, M., Wada, H., Ito, M., Nakano, T., Sasaki, Y., Narumiya, S., Shiku, H., Nishikawa, M. Blood (1999) [Pubmed]
  28. The G protein-coupled receptor S1P2 regulates Rho/Rho kinase pathway to inhibit tumor cell migration. Lepley, D., Paik, J.H., Hla, T., Ferrer, F. Cancer Res. (2005) [Pubmed]
  29. Regulation of tight junction permeability and occludin phosphorylation by Rhoa-p160ROCK-dependent and -independent mechanisms. Hirase, T., Kawashima, S., Wong, E.Y., Ueyama, T., Rikitake, Y., Tsukita, S., Yokoyama, M., Staddon, J.M. J. Biol. Chem. (2001) [Pubmed]
  30. RhoA/ROCK signaling regulates Sox9 expression and actin organization during chondrogenesis. Woods, A., Wang, G., Beier, F. J. Biol. Chem. (2005) [Pubmed]
  31. The functional role of rho and rho-associated coiled-coil forming protein kinase in eotaxin signaling of eosinophils. Adachi, T., Vita, R., Sannohe, S., Stafford, S., Alam, R., Kayaba, H., Chihara, J. J. Immunol. (2001) [Pubmed]
  32. Effects of Peripheral Cannabinoid Receptor Ligands on Motility and Polarization in Neutrophil-like HL60 Cells and Human Neutrophils. Kurihara, R., Tohyama, Y., Matsusaka, S., Naruse, H., Kinoshita, E., Tsujioka, T., Katsumata, Y., Yamamura, H. J. Biol. Chem. (2006) [Pubmed]
  33. RhoA modulates Smad signaling during transforming growth factor-beta-induced smooth muscle differentiation. Chen, S., Crawford, M., Day, R.M., Briones, V.R., Leader, J.E., Jose, P.A., Lechleider, R.J. J. Biol. Chem. (2006) [Pubmed]
  34. Cell type-specific regulation of RhoA activity during cytokinesis. Yoshizaki, H., Ohba, Y., Parrini, M.C., Dulyaninova, N.G., Bresnick, A.R., Mochizuki, N., Matsuda, M. J. Biol. Chem. (2004) [Pubmed]
  35. Rho kinase: a target for treating urinary bladder dysfunction? Peters, S.L., Schmidt, M., Michel, M.C. Trends Pharmacol. Sci. (2006) [Pubmed]
  36. Intrahepatic upregulation of RhoA and Rho-kinase signalling contributes to increased hepatic vascular resistance in rats with secondary biliary cirrhosis. Zhou, Q., Hennenberg, M., Trebicka, J., Jochem, K., Leifeld, L., Biecker, E., Sauerbruch, T., Heller, J. Gut (2006) [Pubmed]
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