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Search results for "Pharmacologic Substance[C1909]|Agent Affecting Cardiovascular System[C78274]" in comments (approximate match)
Status:
US Previously Marketed
Source:
TEVETEN HCT by ABBVIE
(2001)
Source URL:
First approved in 1997
Source:
TEVETEN by ABBVIE
Source URL:
Class (Stereo):
CHEMICAL (ACHIRAL)
Conditions:
Eprosartan is an angiotensin II receptor antagonist used for the treatment of high blood pressure. It acts on the renin-angiotensin system in two ways to decrease total peripheral resistance. First, it blocks the binding of angiotensin II to AT1 receptors in vascular smooth muscle, causing vascular dilatation. Second, it inhibits sympathetic norepinephrine production, further reducing blood pressure. Eprosartan is indicated for the management of hypertension alone or in combination with other classes of antihypertensive agents. Also used as a first-line agent in the treatment of diabetic nephropathy, as well as a second-line agent in the treatment of congestive heart failure (only in those intolerant of ACE inhibitors).
Status:
US Previously Marketed
Source:
RENORMAX by SCHERING
(1994)
Source URL:
First approved in 1994
Source:
RENORMAX by SCHERING
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Targets:
Conditions:
Spirapril (Renormax) is an ACE inhibitor antihypertensive drug used to treat hypertension. Spiraprilat, the active metabolite of spirapril, competes with angiotensin I for binding at the angiotensin-converting enzyme, blocking the conversion of angiotensin I to angiotensin II. Inhibition of ACE results in decreased plasma angiotensin II. As angiotensin II is a vasoconstrictor and a negative-feedback mediator for renin activity, lower concentrations result in a decrease in blood pressure and stimulation of baroreceptor reflex mechanisms, which leads to decreased vasopressor activity and to decreased aldosterone secretion. Spiraprilat may also act on kininase II, an enzyme identical to ACE that degrades the vasodilator bradykinin.
Status:
First approved in 1992
Class (Stereo):
CHEMICAL (UNKNOWN)
Targets:
Conditions:
Flosequinan is a vasodilator developed for the treatment of heart failure. The drug was marketed under the name Manoplax, however it was withdrawn by the FDA decision since it increased congestive heart failure symptoms. The exact mechanism of flosequinan action is unknown, but there are studies reporting the inhibition of PDE3 activity.
Status:
US Previously Marketed
Source:
ETHMOZINE by SHIRE
(1990)
Source URL:
First approved in 1990
Source:
ETHMOZINE by SHIRE
Source URL:
Class (Stereo):
CHEMICAL (ACHIRAL)
Conditions:
Moricizine is an antiarrhythmic agent previously marketed as Ethmozine. It was used for prophylaxis and treatment of serious and life-threatening ventricular arrhythmias. In 2007 it was withdrawn and discontinued for commercial reasons. Moricizine can be administered intravenously but was more commonly provided as an oral formulation.
Status:
US Previously Marketed
Source:
PINDAC by LEO PHARM
(1989)
Source URL:
First approved in 1989
Source:
PINDAC by LEO PHARM
Source URL:
Class (Stereo):
CHEMICAL (RACEMIC)
Targets:
Conditions:
Pinacidil is a clinically effective vasodilator used for the treatment of hypertension.
Status:
US Previously Marketed
Source:
DECABID by LILLY
(1989)
Source URL:
First approved in 1989
Source:
DECABID by LILLY
Source URL:
Class (Stereo):
CHEMICAL (ACHIRAL)
Targets:
Indecainide, an antiarrhythmic agent classified as type IC. Class IC drugs greatly depress intracardiac conduction and are the most potent antiarrhythmic compounds able to suppress ventricular premature beats. Indecainide was used under brand name decabid for the treatment of life-threatening dysrhythmias and sustained ventricular tachycardia. However, that usage was discontinued. Indecainide have mediated the pharmacological actions through a blocking of Na+-channel.
Status:
First approved in 1986
Class (Stereo):
CHEMICAL (RACEMIC)
Conditions:
Encainide is an antiarrhythmic drug, developed by Bristol Myers Co supplied 25 and 35 mg capsules for oral administration. Encainide is no longer used because of its frequent proarrhythmic side effects. The mechanisms of the antiarrhythmic effects of Enkaid are unknown but probably are the result of its ability to slow conduction, reduce membrane responsiveness, inhibit automaticity, and increase the ratio of the effective refractory period to action potential duration. Enkaid produces a differentially greater effect on the ischemic zone as compared with normal cells in the myocardium. This could result in the elimination of the disparity in the electrophysiologic properties between these two zones and eliminate pathways of abnormal impulse conduction, development of boundary currents and/or sites of abnormal impulse generation. The absorption of Enkaid after oral administration is nearly complete with peak plasma levels present 30 to 90 minutes after dosing. There are two major genetically determined patterns of encainide metabolism. In over 90% of patients, the drug is rapidly and extensively metabolized with an elimination half-life of 1 to 2 hours. These patients convert encainide to two active metabolites, O-demethylencainide (ODE) and 3-methoxy-O-demethylencainide (MODE), that are more active (on a per mg basis) than encainide itself. In less than 10% of patients, metabolism of encainide is slower and the estimated encainide elimination half-life is 6 to 11 hours. Slow metabolism of encainide is associated with a diminished ability to metabolize debrisoquin. Enkaid should be administered only after appropriate clinical assessment and the dosage of Enkaid must be individualized for each patient on the basis of therapeutic response and tolerance. The recommended initial dosing schedule for adults is one 25 mg Enkaid capsule t.i.d. at approximately 8-hour intervals.
Status:
US Previously Marketed
Source:
TONOCARD by ASTRAZENECA
(1984)
Source URL:
First approved in 1984
Source:
TONOCARD by ASTRAZENECA
Source URL:
Class (Stereo):
CHEMICAL (RACEMIC)
Targets:
Conditions:
Tocainide is a primary amine analog of lidocaine with antiarrhythmic properties useful in the treatment of ventricular arrhythmias. Tocainide, like lidocaine, produces dose-dependent decreases in sodium and potassium conductance, thereby decreasing the excitability of myocardial cells. In experimental animal models, the dose-related depression of sodium current is more pronounced in ischemic tissue than in normal tissue. Tocainide is a Class I antiarrhythmic compound with electrophysiologic properties in man similar to those of lidocaine, but dissimilar from quinidine, procainamide, and disopyramide. The recommended initial dosage is 400 mg every 8 hours. The usual adult dosage is between 1200 and 1800 mg/day in a three-dose daily divided regimen. Doses beyond 2400 mg per day have been administered infrequently. Patients who tolerate the t.i.d. the regimen may be tried on a twice-daily regimen with careful monitoring. Tocainide commonly produces minor, transient, nervous system and gastrointestinal adverse reactions, but is otherwise generally well tolerated.
Status:
US Previously Marketed
Source:
HYLOREL by PHARMACIA AND UPJOHN
(1982)
Source URL:
First approved in 1982
Source:
HYLOREL by PHARMACIA AND UPJOHN
Source URL:
Class (Stereo):
CHEMICAL (RACEMIC)
Conditions:
Guanadrel is a postganglionic adrenergic blocking agent. Uptake of guanadrel and storage in sympathetic neurons occurs via the norepinephrine pump or transporter. Guanadrel slowly displaces norepinephrine from its storage in nerve endings and thereby blocks the release of norepinephrine normally produced by nerve stimulation. The reduction in neurotransmitter release in response to sympathetic nerve stimulation, as a result of catecholamine depletion, leads to reduced arteriolar vasoconstriction, especially the reflex increase in sympathetic tone that occurs with a change in position. Guanadrel is used to treat and control hypertension.
Status:
US Previously Marketed
Source:
ISMOTIC by ALCON
(1974)
Source URL:
First approved in 1974
Source:
ISMOTIC by ALCON
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Conditions:
Isosorbide is an effective hyperosmotic agent which can be administered orally without gastrointestinal irritation. It is absorbed quantitatively and more than 95% of the administered dose is excreted unchanged in the urine. Oral administration of a 50% solution to rabbits or man results in prompt increases in osmolarity of the serum and profound decreases in intraocular pressure. The drug proves useful in acute primary and secondary glaucomas, and as preoperative medication for various surgical procedures including cataract extraction, retinal detachment, corneal transplant, and glaucoma operations.