{{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}}
{{facet.count}}
{{facet.count}}
{{facet.count}}
{{facet.count}}
{{facet.count}}
{{facet.count}}
Restrict the search for
vitamin a
to a specific field?
Status:
US Approved Rx
(2017)
Source:
ANDA208820
(2017)
Source URL:
First approved in 1981
Source:
NADA111607
Source URL:
Class (Stereo):
CHEMICAL (RACEMIC)
Targets:
Conditions:
Praziquantel, marketed as Biltricide, is an anthelmintic used in humans and animals for the treatment of tapeworms and flukes. Specifically, it is effective against schistosoma, Clonorchis sinensis the fish tape worm Diphyllobothrium latum. Praziquantel works by causing severe spasms and paralysis of the worms' muscles. This paralysis is accompanied - and probably caused - by a rapid Ca 2+ influx inside the schistosome. Morphological alterations are another early effect of praziquantel. These morphological alterations are accompanied by an increased exposure of schistosome antigens at the parasite surface. The worms are then either completely destroyed in the intestine or passed in the stool. An interesting quirk of praziquantel is that it is relatively ineffective against juvenile schistosomes. While initially effective, effectiveness against schistosomes decreases until it reaches a minimum at 3-4 weeks. Effectiveness then increases again until it is once again fully effective at 6-7 weeks. Glutathione S-transferase (GST), an essential detoxification enzyme in parasitic helminths, is a major vaccine target and a drug target against schistosomiasis. Schistosome calcium ion channels are currently the only known target of praziquantel. The antibiotic rifampicin decreases plasma concentrations of praziquantel. Carbamazepine and phenytoin are reported to reduce the bioavailability of praziquantel. Chloroquine reduces the bioavailability of praziquantel. The drug cimetidine heightens praziquantel bioavailability.
Status:
US Approved Rx
(2016)
Source:
ANDA205390
(2016)
Source URL:
First approved in 1981
Class (Stereo):
CHEMICAL (ABSOLUTE)
Conditions:
Vecuronium is a neuromuscular blocking agent. Vecuronium operates by competing for the cholinoceptors at the motor end plate thereby exerting its muscle-relaxing properties which are used adjunctively to general anesthesia. Vecuronium is a bisquaternary nitrogen compound that acts by competitively binding to nicotinic cholinergic receptors. The binding of vecuronium decreases the opportunity for acetylcholine to bind to the nicotinic receptor at the postjunctional membrane of the myoneural junction. As a result, depolarization is prevented, calcium ions are not released and muscle contraction does not occur. Vecuronium is indicated as an adjunct to general anesthesia, to facilitate endotracheal intubation and to provide skeletal muscle relaxation during surgery or mechanical ventilation.
Status:
US Approved Rx
(2018)
Source:
ANDA207607
(2018)
Source URL:
First approved in 1981
Source:
BUPRENEX by INDIVIOR
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Buprenorphine is an opioid analgesic, used to treat opioid addiction, moderate acute pain, and moderate chronic pain. Buprenorphine is a partial agonist at the mµ-opioid receptor and an antagonist at the kappa-opioid receptor. One unusual property of buprenorphine observed in vitro studies is its very slow rate of dissociation from its receptor. This could account for its longer duration of action than morphine, the unpredictability of its reversal by opioid antagonists, and its low level of manifest physical dependence. The principal action of the therapeutic value of buprenorphine is analgesia and is thought to be due to buprenorphine binding with high affinity to opioid receptors on neurons in the brain and spinal cord. Buprenorphine produces respiratory depression by direct action on brain stem respiratory centers. The respiratory depression involves a reduction in the responsiveness of the brain stem respiratory centers to both increases in carbon dioxide tension and electrical stimulation. Buprenorphine causes a reduction in motility associated with an increase in smooth muscle tone in the antrum of the stomach and duodenum. Digestion of food in the small intestine is delayed and propulsive contractions are decreased. Buprenorphine produces peripheral vasodilation, which may result in orthostatic hypotension or syncope. Manifestations of histamine release and/or peripheral vasodilation may include pruritus, flushing, red eyes, sweating, and/or orthostatic hypotension.
Status:
US Approved Rx
(2013)
Source:
ANDA202180
(2013)
Source URL:
First approved in 1981
Source:
DESYREL by PRAGMA
Source URL:
Class (Stereo):
CHEMICAL (ACHIRAL)
Targets:
Trazodone (brand name Oleptro, Desyrel, etc) is a serotonin uptake inhibitor that is used as an antidepressive agent. Trazodone binds to the 5-HT2 receptor, it acts as a serotonin agonist at high doses and a serotonin antagonist at low doses. Like fluoxetine, trazodone's antidepressant activity likely results from blockage of serotonin reuptake by inhibiting serotonin reuptake pump at the presynaptic neuronal membrane. If used for long time periods, postsynaptic neuronal receptor binding sites may also be affected. The sedative effect of trazodone is likely the result of alpha-adrenergic blocking action and modest histamine blockade at the H1 receptor. It weakly blocks presynaptic alpha2-adrenergic receptors and strongly inhibits postsynaptic alpha1 receptors. Trazodone does not affect the reuptake of norepinephrine or dopamine within the CNS. Because of its lack of anticholinergic side effects, trazodone is especially useful in situations in which antimuscarinic effects are particularly problematic (e.g., in patients with benign prostatic hyperplasia, closed-angle glaucoma, or severe constipation). Trazodone's propensity to cause sedation is a dual-edged sword. For many patients, the relief from agitation, anxiety, and insomnia can be rapid; for other patients, including those individuals with considerable psychomotor retardation and feelings of low energy, therapeutic doses of trazodone may not be tolerable because of sedation. Trazodone elicits orthostatic hypotension in some patients, probably as a consequence of α1-adrenergic receptor blockade. Mania has been observed in association with trazodone treatment, including in patients with bipolar disorder, as well as in patients with previous diagnoses of major depression. Compared to the reversible MAOI antidepressant drug moclobemide, significantly more impairment of vigilance occurs with trazodone.
Status:
US Approved Rx
(2016)
Source:
NDA208010
(2016)
Source URL:
First approved in 1980
Source:
CALDEROL by ORGANON USA INC
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Targets:
Conditions:
Calcifediol (25-Hydroxyvitamin D3 or 25-hydroxycholecalciferol) is a biologically active vitamin D3 metabolite. It is concluded that the liver is the major if not the only physiologic site of hydroxylation of vitamin D3 into calcifediol. Calcifediol is a prohormone of the active form of vitamin D3, calcitriol (1,25-dihydroxyvitamin D3). Calcifediol is converted to calcitriol by cytochrome P450 27B1 (CYP27B1), also called 1-alpha hydroxylase, primarily in the kidney. Calcitriol binds to the vitamin D receptor in target tissues and activates vitamin D responsive pathways that result in increased intestinal absorption of calcium and phosphorus and reduced parathyroid hormone synthesis. RAYALDEE (calcifediol) extended-release capsules is indicated for the treatment of secondary hyperparathyroidism in adult patients with stage 3 or 4 chronic kidney disease.
Status:
US Approved Rx
(1998)
Source:
NDA050731
(1998)
Source URL:
First approved in 1979
Source:
CERUBIDINE by WYETH AYERST
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Targets:
Daunorubicin, also known as daunomycin, is a chemotherapy medication used to treat cancer. Specifically, it is used for acute myeloid leukemia (AML), acute lymphocytic leukemia (ALL), chronic myelogenous leukemia (CML), and Kaposi's sarcoma. Similar to doxorubicin, daunorubicin interacts with DNA by intercalation and inhibition of macromolecular biosynthesis. This inhibits the progression of the enzyme topoisomerase II, which relaxes supercoils in DNA for transcription. Daunorubicin stabilizes the topoisomerase II complex after it has broken the DNA chain for replication, preventing the DNA double helix from being resealed and thereby stopping the process of replication. On binding to DNA, daunomycin intercalates, with its daunosamine residue directed toward the minor groove. It has the highest preference for two adjacent G/C base pairs flanked on the 5' side by an A/T base pair. Daunorubicin should only be administered in a rapid intravenous infusion. It should not be administered intramuscularly or subcutaneously, since it may cause extensive tissue necrosis. It should also never be administered intrathecally (into the spinal canal), as this will cause extensive damage to the nervous system and may lead to death.
Status:
US Approved Rx
(2016)
Source:
ANDA208127
(2016)
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
(1979)
Source:
NDA017624
(1979)
Source URL:
First approved in 1979
Source:
NDA017624
Source URL:
Class (Stereo):
CHEMICAL (RACEMIC)
Conditions:
Isoflurane (1-chloro-2, 2,2-trifluoroethyl difluoromethyl ether) a nonflammable liquid administered by vaporizing, is a general inhalation anesthetic drug. Isoflurane is a clear, colorless, stable liquid containing no additives or chemical stabilizers. Similar to many general anesthetics, the exact mechanism of the action has not been clearly delineated. Isoflurane reduces pain sensitivity (analgesia) and relaxes muscles. Isoflurane likely potentiates GABA-A and glycine receptor activity, which decreases motor function, inhibits receptor activity in the NMDA glutamate receptor subtypes and binds to glutamate receptors. Isoflurane is always administered in conjunction with air and/or pure oxygen. Often nitrous oxide is also used. Although its physical properties imply that anesthesia can be induced more rapidly than with halothane, its pungency can irritate the respiratory system, negating this theoretical advantage conferred by its physical properties. It is usually used to maintain a state of general anesthesia that has been induced with another drug, such as thiopentone or propofol.
Status:
US Approved Rx
(2008)
Source:
ANDA078807
(2008)
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:
ANDA078085
(2008)
Source URL:
First approved in 1978
Source:
NDA017963
Source URL:
Class (Stereo):
CHEMICAL (RACEMIC)
Targets:
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
