Platelet inhibitory effects of the NO independent sGC stimulator riociguat (Bay 63-2561)
نویسندگان
چکیده
منابع مشابه
Discovery of riociguat (BAY 63-2521): a potent, oral stimulator of soluble guanylate cyclase for the treatment of pulmonary hypertension
Soluble guanylate cyclase (sGC) is a key signal-transduction enzyme activated by nitric oxide (NO). Impairments of the NO-sGC signaling pathway have been implicated in the pathogenesis of cardiovascular and other diseases. Direct stimulation of sGC represents a promising therapeutic strategy particularly for the treatment of pulmonary hypertension (PH), a disabling disease associated with a poo...
متن کاملNo pharmacodynamic (PD) and pharmacokinetic (PK) interaction of riociguat (BAY 63-2521) and aspirin
Objectives Riociguat, an oral soluble guanylate cyclase (sGC) stimulator, is a new candidate for treatment of pulmonary hypertension (PH). Riociguat increases cGMP production through a novel dual mode of action: direct NOindependent stimulation of sGC and increasing sensitivity of sGC to low levels of NO. Another sGC stimulator, BAY 41-2272, has shown anti-platelet activity in animal models, as...
متن کاملWarfarin pharmacodynamics and pharmacokinetics are not affected by the soluble guanylate cyclase stimulator riociguat (BAY 63-2521)
Background Pulmonary hypertension (PH) is a progressive and debilitating condition with a high rate of mortality. Riociguat (BAY 63-2521) is a new drug in development for PH that is well tolerated [1,2] and has superior efficacy to nitric oxide in patients with PH [2]. Treatment recommendations for PH are based on combination therapies that include warfarin. The aim of this study was to investi...
متن کاملEffects of the sGC Stimulator BAY 41-2272 Are Not Mediated by Phosphodiesterase 5 Inhibition
Not Mediated by Phosphodiesterase 5 Inhibition To the Editor: A major conclusion of the recent publication of Mullershausen et al1 is that “the physiological effects of BAY 41-2272 . . . are due to the synergism of sensitization of NO-sensitive GC [guanylate cyclase] and inhibition of PDE5.” This conclusion is based on the authors’ finding that BAY 41-2272 stimulates sGC and inhibits human PDE5...
متن کاملEffects of the sGC stimulator BAY 41-2272 are not mediated by phosphodiesterase 5 inhibition.
Not Mediated by Phosphodiesterase 5 Inhibition To the Editor: A major conclusion of the recent publication of Mullershausen et al1 is that “the physiological effects of BAY 41-2272 . . . are due to the synergism of sensitization of NO-sensitive GC [guanylate cyclase] and inhibition of PDE5.” This conclusion is based on the authors’ finding that BAY 41-2272 stimulates sGC and inhibits human PDE5...
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ژورنال
عنوان ژورنال: BMC Pharmacology and Toxicology
سال: 2013
ISSN: 2050-6511
DOI: 10.1186/2050-6511-14-s1-p55