BAY 41-2272 has been used for the stimulation of guanylate cyclase in heart[1] and neurons.[2]
Biochem/physiol Actions
BAY 41-2272 is an activator of soluble guanylate cyclase at a novel, NO-independent regulatory site. BAY 41-2272 is the first product that stimulates sGC through a non-NO mechanism. BAY 41-2272 inhibits platelet aggregation and induces vasorelaxation without nitrate tolerance.
BAY 41-2272 is an activator of soluble guanylate cyclase; stimulates sGC through a non-NO mechanism; inhibits platelet aggregation, and induces vasorelaxation without nitrate tolerance.
Features and Benefits
This compound was developed by Bayer. To browse the list of other pharma-developed compounds and Approved Drugs/Drug Candidates, click here.
In the hippocampus, as in many other CNS areas, nitric oxide (NO) participates in synaptic plasticity, manifested as changes in pre- and/or postsynaptic function. While it is known that these changes are brought about by cGMP following activation of guanylyl
Adiposity greatly increases the risk of atherothrombotic events, a pathological condition where a chronic state of oxidative stress is reported to play a major role. This study aimed to investigate the involvement of (NO)-soluble guanylyl cyclase (sGC) signaling pathway in
Journal of pharmacological sciences, 125(2), 169-175 (2014-05-27)
Hypoxia or hypoxia/reoxygenation impairs nitric oxide (NO)-mediated relaxation through the increase in superoxide generation in monkey coronary arteries. Soluble guanylate cyclase (sGC), the target enzyme of NO, has been shown to change from the NO-sensitive reduced form to the NO-insensitive
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Sepsis and septic shock are associated with high mortality rates and the majority of sepsis patients die due to complications of multiple organ failure (MOF). The cyclic GMP (cGMP) producing enzyme soluble guanylate cyclase (sGC) is crucially involved in the
DISCOVER Bioactive Small Molecules for Nitric Oxide & Cell Stress Research
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