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Year Number of Results
2002 1
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2009 14
2010 8
2011 11
2012 11
2013 11
2014 7
2015 10
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128 results

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Page 1
BAY 58-2667, a nitric oxide-independent guanylyl cyclase activator, pharmacologically post-conditions rabbit and rat hearts.
Krieg T, Liu Y, Rütz T, Methner C, Yang XM, Dost T, Felix SB, Stasch JP, Cohen MV, Downey JM. Krieg T, et al. Eur Heart J. 2009 Jul;30(13):1607-13. doi: 10.1093/eurheartj/ehp143. Epub 2009 Apr 30. Eur Heart J. 2009. PMID: 19406872
AIMS: BAY 58-2667 (BAY-58) directly activates soluble guanylyl cyclase without tolerance in a nitric oxide (NO)-independent manner, and its haemodynamic effect is similar to that of nitroglycerin. ...
AIMS: BAY 58-2667 (BAY-58) directly activates soluble guanylyl cyclase without tolerance in a nitric oxide (NO)-indepen …
The soluble guanylyl cyclase activator bay 58-2667 selectively limits cardiomyocyte hypertrophy.
Irvine JC, Ganthavee V, Love JE, Alexander AE, Horowitz JD, Stasch JP, Kemp-Harper BK, Ritchie RH. Irvine JC, et al. PLoS One. 2012;7(11):e44481. doi: 10.1371/journal.pone.0044481. Epub 2012 Nov 7. PLoS One. 2012. PMID: 23144773 Free PMC article.
In the present study, we tested the hypothesis that the NO()-independent sGC activator BAY 58-2667 inhibits cardiomyocyte hypertrophy in vitro. Concomitant impact of BAY 58-2667 on cardiac fibroblast proliferation, and insights into poten …
In the present study, we tested the hypothesis that the NO()-independent sGC activator BAY 58-2667 inhibits cardiomyocy …
Structure of cinaciguat (BAY 58-2667) bound to Nostoc H-NOX domain reveals insights into heme-mimetic activation of the soluble guanylyl cyclase.
Martin F, Baskaran P, Ma X, Dunten PW, Schaefer M, Stasch JP, Beuve A, van den Akker F. Martin F, et al. J Biol Chem. 2010 Jul 16;285(29):22651-7. doi: 10.1074/jbc.M110.111559. Epub 2010 May 12. J Biol Chem. 2010. PMID: 20463019 Free PMC article.
Here, we present crystallographic and mutagenesis data that reveal the mode of action of BAY 58-2667. The 2.3-A resolution structure of BAY 58-2667 bound to a heme NO and oxygen binding domain (H-NOX) from Nostoc homologous to that of sGC …
Here, we present crystallographic and mutagenesis data that reveal the mode of action of BAY 58-2667. The 2.3-A resolut …
Anti-aggregating effect of BAY 58-2667, an activator of soluble guanylyl cyclase.
Roger S, Paysant J, Badier-Commander C, Cordi A, Verbeuren TJ, Félétou M. Roger S, et al. Vascul Pharmacol. 2010 Nov-Dec;53(5-6):281-7. doi: 10.1016/j.vph.2010.09.008. Epub 2010 Oct 7. Vascul Pharmacol. 2010. PMID: 20933607
The inhibitor of sGC, ODQ, enhanced the effects of BAY 58-2667. The presence of L-nitroarginine, an inhibitor of NO-synthase, hydroxocobalamin, a scavenger of NO, or that of three different NO-donors did not affect the anti-aggregating effect of BAY
The inhibitor of sGC, ODQ, enhanced the effects of BAY 58-2667. The presence of L-nitroarginine, an inhibitor of NO-syn …
The soluble guanylate cyclase activator BAY 58-2667 protects against morbidity and mortality in endotoxic shock by recoupling organ systems.
Vandendriessche B, Rogge E, Goossens V, Vandenabeele P, Stasch JP, Brouckaert P, Cauwels A. Vandendriessche B, et al. PLoS One. 2013 Aug 28;8(8):e72155. doi: 10.1371/journal.pone.0072155. eCollection 2013. PLoS One. 2013. PMID: 24015214 Free PMC article.
The resulting heme-free sGC can be reactivated by the heme- and nitric oxide (NO)-independent sGC activator BAY 58-2667 (Cinaciguat). We report that late (+8 h) post-treatment with BAY 58-2667 in a mouse model can protect against lethal e …
The resulting heme-free sGC can be reactivated by the heme- and nitric oxide (NO)-independent sGC activator BAY 58-2667
Activation of soluble guanylyl cyclase by BAY 58-2667 improves bladder function in cyclophosphamide-induced cystitis in mice.
de Oliveira MG, Calmasini FB, Alexandre EC, De Nucci G, Mónica FZ, Antunes E. de Oliveira MG, et al. Am J Physiol Renal Physiol. 2016 Jul 1;311(1):F85-93. doi: 10.1152/ajprenal.00041.2016. Epub 2016 Apr 27. Am J Physiol Renal Physiol. 2016. PMID: 27122537 Free article.
This study aimed to evaluate the effects of the sGC activator BAY 58-2667 on voiding dysfunction, protein expressions of alpha1 and beta1 sGC subunits and cGMP levels in the bladder tissues after cyclophosphamide (CYP) exposure. ...Reduced protein expressions …
This study aimed to evaluate the effects of the sGC activator BAY 58-2667 on voiding dysfunction, protein expressions o …
Cinaciguat (BAY 58-2667) improves cardiopulmonary hemodynamics in patients with acute decompensated heart failure.
Lapp H, Mitrovic V, Franz N, Heuer H, Buerke M, Wolfertz J, Mueck W, Unger S, Wensing G, Frey R. Lapp H, et al. Circulation. 2009 Jun 2;119(21):2781-8. doi: 10.1161/CIRCULATIONAHA.108.800292. Epub 2009 May 18. Circulation. 2009. PMID: 19451356 Clinical Trial.
BACKGROUND: Cinaciguat (BAY 58-2667) is the first of a new class of soluble guanylate cyclase activators in clinical development for acute decompensated heart failure. ...
BACKGROUND: Cinaciguat (BAY 58-2667) is the first of a new class of soluble guanylate cyclase activators in clinical de …
Human trabecular meshwork cell volume decrease by NO-independent soluble guanylate cyclase activators YC-1 and BAY-58-2667 involves the BKCa ion channel.
Dismuke WM, Sharif NA, Ellis DZ. Dismuke WM, et al. Invest Ophthalmol Vis Sci. 2009 Jul;50(7):3353-9. doi: 10.1167/iovs.08-3127. Epub 2009 Feb 21. Invest Ophthalmol Vis Sci. 2009. PMID: 19234350
RESULTS: YC-1 (10 nM-200 microM) and BAY-58-2667 (10 nM-100 microM) each elicited a biphasic effect on TM cell volume. YC-1 (1 microM) increased TM cell volume, but higher concentrations decreased TM cell volume. Similarly, BAY-58-2667 (1 …
RESULTS: YC-1 (10 nM-200 microM) and BAY-58-2667 (10 nM-100 microM) each elicited a biphasic effect on TM cell volume. …
Pharmacokinetics, pharmacodynamics, tolerability, and safety of the soluble guanylate cyclase activator cinaciguat (BAY 58-2667) in healthy male volunteers.
Frey R, Mück W, Unger S, Artmeier-Brandt U, Weimann G, Wensing G. Frey R, et al. J Clin Pharmacol. 2008 Dec;48(12):1400-10. doi: 10.1177/0091270008322906. Epub 2008 Sep 8. J Clin Pharmacol. 2008. PMID: 18779378 Clinical Trial.
Preclinical data indicate that the nitric oxide-independent soluble guanylate cyclase activator cinaciguat (BAY 58-2667), which is a new drug in development for patients with heart failure, induces vasodilation preferentially in diseased vessels. ...
Preclinical data indicate that the nitric oxide-independent soluble guanylate cyclase activator cinaciguat (BAY 58-2667
NO-independent, haem-dependent soluble guanylate cyclase stimulators.
Stasch JP, Hobbs AJ. Stasch JP, et al. Handb Exp Pharmacol. 2009;(191):277-308. doi: 10.1007/978-3-540-68964-5_13. Handb Exp Pharmacol. 2009. PMID: 19089334 Review.
In contrast to the NO- and haem-independent sGC activators such as BAY 58-2667, these compounds stimulate sGC activity independent of NO and also act in synergy with NO to produce anti-aggregatory, anti-proliferative, and vasodilatory effects. ...
In contrast to the NO- and haem-independent sGC activators such as BAY 58-2667, these compounds stimulate sGC activity …
128 results