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Restrict the search for
dopamine
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Status:
US Approved Rx
(2015)
Source:
ANDA204521
(2015)
Source URL:
First approved in 1984
Source:
ORAP by TEVA
Source URL:
Class (Stereo):
CHEMICAL (ACHIRAL)
Targets:
Conditions:
Pimozide (Orap) is a diphenylbutylpiperidine that is effective as an antipsychotic agent and as an alternative to haloperidol for the suppression of vocal and motor tics in patients with Tourette syndrome. It is not intended as a treatment of first choice nor is it intended for the treatment of tics that are merely annoying or cosmetically troublesome. It should be reserved for use in Tourette’s Disorder patients whose development and/or daily life function is severely compromised by the presence of motor and phonic tics. Evidence supporting approval of pimozide for use in Tourette’s Disorder was obtained in two controlled clinical investigations, which enrolled patients between the ages of 8 and 53 years. Most subjects in the two trials were 12 or older. Pimozide is an orally active antipsychotic drug product, which shares with other antipsychotics the ability to blockade dopaminergic receptors on neurons in the central nervous system. Although its exact mode of action has not been established, the ability of pimozide to suppress motor and phonic tics in Tourette’s Disorder is thought to be a function of its dopaminergic blocking activity. However, receptor blockade is often accompanied by a series of secondary alterations in central dopamine metabolism and function which may contribute to both pimozide’s therapeutic and untoward effects. In addition, pimozide, in common with other antipsychotic drugs, has various effects on other central nervous system receptor systems which are not fully characterized.
Status:
US Approved Rx
(1992)
Source:
ANDA072691
(1992)
Source URL:
First approved in 1980
Source:
ASENDIN by LEDERLE
Source URL:
Class (Stereo):
CHEMICAL (ACHIRAL)
Amoxapine is an antidepressant of the dibenzoxazepine class, chemically distinct from the dibenzazepines, dibenzocycloheptenes, and dibenzoxepines. It is designated chemically as 2-Chloro-11- (1-piperazinyl)dibenz[b,f ][1,4]oxazepine. Amoxapine is an antidepressant with a mild sedative component to its action. The mechanism of its clinical action in man is not well understood. In animals, amoxapine reduced the uptake of norepinephrine and serotonin and blocked the response of dopamine receptors to dopamine. Amoxapine is not a monoamine oxidase inhibitor. Amoxapine is absorbed rapidly and reaches peak blood levels approximately 90 minutes after ingestion. It is almost completely metabolized. The main route of excretion is the kidney. In vitro tests show that amoxapine binding to human serum is approximately 90%. In man, amoxapine serum concentration declines with a half-life of eight hours. However, the major metabolite, 8-hydroxyamoxapine, has a biologic half-life of 30 hours. Metabolites are excreted in the urine in conjugated form as glucuronides. Clinical studies have demonstrated that amoxapine has a more rapid onset of action than either amitriptyline or imipramine. The initial clinical effect may occur within four to seven days and occurs within two weeks in over 80% of responders.
Status:
US Approved Rx
(2006)
Source:
ANDA077361
(2006)
Source URL:
First approved in 1979
Source:
SURMONTIL by ODYSSEY PHARMS
Source URL:
Class (Stereo):
CHEMICAL (RACEMIC)
Conditions:
Trimipramine is a tricyclic antidepressant similar to imipramine, but with more antihistaminic and sedative properties. It was sold under brand name surmontil for the relief of symptoms of depression. Endogenous depression is more likely to be alleviated than other depressive states. In studies with neurotic outpatients, the drug appeared to be equivalent to amitriptyline in the less-depressed patients but somewhat less effective than amitriptyline in the more severely depressed patients. In hospitalized depressed patients, trimipramine and imipramine were equally effective in relieving depression. Trimipramine has been reported to differ from other typical tricyclic antidepressant drugs in several aspects, for instance it does not inhibit neuronal transmitter uptake and does not cause down-regulation of beta-adrenoceptors. Moreover, it may possess antipsychotic activity in schizophrenic patients. In addition, was found that it did not antagonize the inhibitory effect of noradrenaline and 5-hydroxytryptamine on the release of transmitter, mediated by presynaptic auto receptors. In radioligand binding studies, trimipramine showed fairly high affinities for some dopamine (DA), noradrenaline and 5-hydroxytryptamine (5-HT) receptor subtypes (5-HT2 receptors = alpha 1A/B-adrenoceptors greater than or equal to D2 receptors), intermediate affinities for D1 receptors, alpha 2B-adrenoceptors and 5-HT1C receptors but only low affinities for alpha 2A-adrenoceptors, 5-HT1A, 5-HT1D and 5-HT3 receptors. It may thus be classified as an atypical neuroleptic drug.
Status:
US Approved Rx
(2020)
Source:
NDA209388
(2020)
Source URL:
First approved in 1979
Source:
REGLAN by HIKMA
Source URL:
Class (Stereo):
CHEMICAL (ACHIRAL)
Targets:
Metoclopramide is a dopamine D2 antagonist that is used as an antiemetic. Metoclopramide inhibits gastric smooth muscle relaxation produced by dopamine, therefore increasing cholinergic response of the gastrointestinal smooth muscle. It accelerates intestinal transit and gastric emptying by preventing relaxation of gastric body and increasing the phasic activity of antrum. Simultaneously, this action is accompanied by relaxation of the upper small intestine, resulting in an improved coordination between the body and antrum of the stomach and the upper small intestine. Metoclopramide also decreases reflux into the esophagus by increasing the resting pressure of the lower esophageal sphincter and improves acid clearance from the esophagus by increasing amplitude of esophageal peristaltic contractions. Metoclopramide's dopamine antagonist action raises the threshold of activity in the chemoreceptor trigger zone and decreases the input from afferent visceral nerves. Studies have also shown that high doses of metoclopramide can antagonize 5-hydroxytryptamine (5-HT) receptors in the peripheral nervous system in animals. Metoclopramide is used for the treatment of gastroesophageal reflux disease (GERD). It is also used in treating nausea and vomiting, and to increase gastric emptying.
Status:
US Approved Rx
(2008)
Source:
ANDA078899
(2008)
Source URL:
First approved in 1978
Source:
NDA017962
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Targets:
Conditions:
Bromocriptine is an ergot derivative with potent dopamine receptor agonist activity, which activates post-synaptic dopamine receptors. Bromocriptine is indicated for the treatment of dysfunctions associated with hyperprolactinemia. Bromocriptine therapy is indicated in the treatment of acromegaly and in the treatment of the signs and symptoms of idiopathic or postencephalitic Parkinson’s disease. It is approved as an adjunct to diet and exercise to improve glycemic control in adults with type 2 diabetes mellitus. Some commonly reported adverse reactions include nausea, fatigue, dizziness, vomiting and headache. Bromocriptine may interact with dopamine antagonists, butyrophenones and certain other agents.
Status:
US Approved Rx
(1988)
Source:
ANDA072206
(1988)
Source URL:
First approved in 1975
Source:
LOXITANE by TEVA BRANDED PHARM
Source URL:
Class (Stereo):
CHEMICAL (ACHIRAL)
Targets:
Loxapine is a dibenzoxazepine tricyclic antipsychotic agent, available for oral and inhalatory administration, classified as a typical antipsychotic. Loxapine acts as an antagonist at central serotonin and dopamine receptors. Adasuve (loxapine inhalation powder) is a prescription medicine that is used to treat acute agitation in adults with schizophrenia or bipolar I disorder.
Status:
US Approved Rx
(2023)
Source:
ANDA217961
(2023)
Source URL:
First approved in 1975
Source:
NDA017555
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Targets:
Conditions:
Carbidopa is a competitive inhibitor of aromatic L-amino acid decarboxylase that does not cross the blood-brain barrier, is routinely administered with levodopa (LD) for the treatment of the symptoms of idiopathic Parkinson’s disease (paralysis agitans), postencephalitic parkinsonism, and symptomatic parkinsonism, which may follow injury to the nervous system by carbon monoxide intoxication and/or manganese intoxication. Current evidence indicates that symptoms of Parkinson’s disease are related to depletion of dopamine in the corpus striatum. Administration of dopamine is ineffective in the treatment of Parkinson’s disease apparently because it does not cross the blood-brain barrier. However, levodopa, the metabolic precursor of dopamine, does cross the blood- brain barrier, and presumably is converted to dopamine in the brain. When levodopa is administered orally it is rapidly decarboxylated to dopamine in extracerebral tissues so that only a small portion of a given dose is transported unchanged to the central nervous system. For this reason, large doses of levodopa are required for adequate therapeutic effect and these may often be accompanied by nausea and other adverse reactions, some of which are attributable to dopamine formed in extracerebral tissues. Carbidopa inhibits decarboxylation of peripheral levodopa. Carbidopa has not been demonstrated to have any overt pharmacodynamic actions in the recommended doses.
Status:
US Approved Rx
(2015)
Source:
ANDA090453
(2015)
Source URL:
First approved in 1974
Source:
MOBAN by CHARTWELL RX
Source URL:
Class (Stereo):
CHEMICAL (RACEMIC)
Conditions:
Molindone (Moban) is a therapeutic antipsychotic, used in the treatment of schizophrenia. The exact mechanism has not been established, however, based on electroencephalogram (EEG) studies, molindone is thought to act by occupying (antagonizing) dopamine (D2) receptor sites in the reticular limbic systems in the brain, thus decreasing dopamine activity. Decreased dopamine activity results in decreased physiological effects normally induced by excessive dopamine stimulation, such as those typically seen in manifestations of psychotic disorders. The side effect profile of molindone is similar to that of other typical antipsychotics. Unlike most antipsychotics, however, molindone use is associated with weight loss.
Status:
US Approved Rx
(1993)
Source:
ANDA074260
(1993)
Source URL:
First approved in 1970
Source:
LARODOPA by ROCHE
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Conditions:
Levodopa (L-DOPA) was first isolated from seedlings of Vicia faba by Marcus Guggenheim in 1913. Levodopa, a dopamine precursor, is an effective and well-tolerated dopamine replacement agent used to treat Parkinson's disease. Oral levodopa has been widely used for over 40 years, often in combination with a dopa-decarboxylase inhibitor carbidopa, which reduces many treatment complications, extending its half-life and increasing levodopa availability to the brain. Entacapone, a catechol-O-methyltransferase inhibitor, can also be used to improve the bioavailability of levodopa, especially when used in conjunction with a carbidopa.
Status:
US Approved Rx
(1988)
Source:
ANDA072123
(1988)
Source URL:
First approved in 1968
Source:
INNOVAR by EPIC PHARMA LLC
Source URL:
Class (Stereo):
CHEMICAL (RACEMIC)
Targets:
Droperidol produces marked tranquilization and sedation. It allays apprehension and provides a state of mental detachment and indifference while maintaining a state of reflex alertness. Droperidol produces an antiemetic effect as evidenced by the antagonism of apomorphine in dogs. It lowers the incidence of nausea and vomiting during surgical procedures and provides antiemetic protection in the postoperative period. Droperidol potentiates other CNS depressants. It produces mild alpha-adrenergic blockade, peripheral vascular dilatation and reduction of the pressor effect of epinephrine. It can produce hypotension and decreased peripheral vascular resistance and may decrease pulmonary arterial pressure (particularly if it is abnormally high). It may reduce the incidence of epinephrine-induced arrhythmias, but it does not prevent other cardiac arrhythmias. The exact mechanism of action is unknown, however, droperidol causes a CNS depression at subcortical levels of the brain, midbrain, and brainstem reticular formation. It may antagonize the actions of glutamic acid within the extrapyramidal system. It may also inhibit cathecolamine receptors and the reuptake of neurotransmiters and has strong central antidopaminergic action and weak central anticholinergic action. It can also produce ganglionic blockade and reduced affective response. The main actions seem to stem from its potent Dopamine (2) receptor antagonism with minor antagonistic effects on alpha-1 adrenergic receptors as well. Droperidol is used to produce tranquilization and to reduce the incidence of nausea and vomiting in surgical and diagnostic procedures.
