U.S. Department of Health & Human Services Divider Arrow National Institutes of Health Divider Arrow NCATS

    {{facet.count}}
    {{facet.count}}

    {{facet.count}}
    {{facet.count}}

    {{facet.count}}
    {{facet.count}}

    {{facet.count}}
    {{facet.count}}

    {{facet.count}}
    {{facet.count}}

    {{facet.count}}
    {{facet.count}}

    {{facet.count}}
    {{facet.count}}

    {{facet.count}}
    {{facet.count}}

    {{facet.count}}
    {{facet.count}}

    {{facet.count}}
    {{facet.count}}

    {{facet.count}}
    {{facet.count}}

    {{facet.count}}
    {{facet.count}}

    {{facet.count}}
    {{facet.count}}

    {{facet.count}}
    {{facet.count}}

    {{facet.count}}
    {{facet.count}}
Mrtoprolol is a beta-adrenergic receptor blocking agent. In vitro and in vivo animal studies have shown that it has a preferential effect on beta-1 adrenoreceptors, chiefly located in cardiac muscle. Clinical pharmacology studies have confirmed the beta-blocking activity of metoprolol in man, as shown by (1) reduction in heart rate and cardiac output at rest and upon exercise, (2) reduction of systolic blood pressure upon exercise, (3) inhibition of isoproterenol-induced tachycardia, and (4) reduction of reflex orthostatic tachycardia. Mrtoprolol is indicated for the treatment of hypertension, angina pectoris and myocardial infarction
Status:
Other

Class (Stereo):
CHEMICAL (ABSOLUTE)



IVABRADINE, (-)- is an (R)-enantiomers of Ivabradine. IVABRADINE, (-)- produced a concentration-dependent block of hKv1.5 channels. S 16260 (R configuration) and S 16257 (S configuration) of Ivabradine were equipotent in reducing the spontaneous firing of rabbit sinus node preparations, but S 16260 induced significant prolongations of action potential duration of ventricular preparation (guinea pig papillary muscle and rabbit purkinje fibers), contrary to S 16257. These in vitro data have been confirmed by in vivo studies in anesthetized pigs showing the equipotence of the two isomers in reducing the heart rate, the absence of effect of S 16257 on the QT interval corrected for heart rate (QTc) in contrast with S 16260 which induced a dose-dependent increase in the QTc, indicating a direct effect on ventricular repolarization.
Status:
Other

Class (Stereo):
CHEMICAL (RACEMIC)

Ivabradine (CORLANOR®) is a hyperpolarization-activated cyclic nucleotide-gated channel blocker that reduces the spontaneous pacemaker activity of the cardiac sinus node by selectively inhibiting the If-current, resulting in heart rate reduction at concentrations that do not affect other cardiac ionic currents. Specific heart-rate lowering with ivabradine (CORLANOR®) reduces myocardial oxygen demand, simultaneously improving oxygen supply. It has no negative inotropic or lusitropic effects, preserving ventricular contractility, and does not change any major electrophysiological parameters unrelated to heart rate.