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Restrict the search for
dimethyl fumarate
to a specific field?
Status:
US Approved Rx
(2016)
Source:
ANDA204068
(2016)
Source URL:
First approved in 1989
Source:
PRILOSEC by ASTRAZENECA
Source URL:
Class (Stereo):
CHEMICAL (RACEMIC)
Targets:
Conditions:
Esomeprazole strontium is a proton pump inhibitor. It suppresses gastric acid secretion by specific inhibition H+/K+ ATPase in the gastric parietal cell. The S- and R-isomers of omeprazole are protonated and converted in the acidic compartment of the parietal cell forming the active inhibitor, the achiral sulphenamide. By acting specifically on the proton pump, esomeprazole blocks the final step in acid production, thus reducing gastric acidity. The drug is indicated for the treatment of gastroesophageal reflux disease, reduction the risk of NSAID-associated gastric ulcer, eradication of H.pylori, and pathological hypersecretory conditions.
Status:
US Approved Rx
(2020)
Source:
ANDA211364
(2020)
Source URL:
First approved in 1989
Source:
NDA019906
Source URL:
Class (Stereo):
CHEMICAL (ACHIRAL)
Targets:
Conditions:
Clomipramine is an antidepressant drug which was approved by FDA for the treatment of Obsessive-Compulsive Disorder. The exact mechanism of its action is unknown, however it is supposed that it may exert its effect by inhibiting serotonin reuptake.
Status:
US Approved Rx
(2024)
Source:
ANDA217548
(2024)
Source URL:
First approved in 1988
Source:
CARDENE by CHIESI
Source URL:
Class (Stereo):
CHEMICAL (RACEMIC)
Targets:
Conditions:
Nicardipine is a potent calcium channel blockader with marked vasodilator action used to treat high blood pressure and angina. By deforming the channel, inhibiting ion-control gating mechanisms, and/or interfering with the release of calcium from the sarcoplasmic reticulum, nicardipine inhibits the influx of extracellular calcium across the myocardial and vascular smooth muscle cell membranes The decrease in intracellular calcium inhibits the contractile processes of the myocardial smooth muscle cells, causing dilation of the coronary and systemic arteries, increased oxygen delivery to the myocardial tissue, decreased total peripheral resistance, decreased systemic blood pressure, and decreased afterload.
Status:
US Approved Rx
(2025)
Source:
ANDA213409
(2025)
Source URL:
First approved in 1988
Source:
NIMOTOP by BAYER PHARMS
Source URL:
Class (Stereo):
CHEMICAL (RACEMIC)
Nimodipine is a dihydropyridine calcium antagonist which has been shown to dilate cerebral arterioles and increase cerebral blood flow in animals and humans. It has potential in the treatment of a range of cerebrovascular disorders. Major interest to date, however, has focused on its use in the prevention and treatment of the delayed ischaemic neurological deficits that frequently occur in patients with subarachnoid haemorrhages as a result of sustained cerebral vasospasm. Nimodipine, a Ca2+ antagonist with cerebrovasodilatory and anti-ischemic effects, binds to rat, guinea pig, and human brain membranes with high affinity (less than 1 nM). Only at higher concentrations has nimodipine been reported to block the release of some neurotransmitters and hormones from neuronal tissue.
Status:
US Approved Rx
(2001)
Source:
ANDA075551
(2001)
Source URL:
First approved in 1987
Source:
MEVACOR by MERCK
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Conditions:
Lovastatin acid is an active metabolite of hypolipidemic drug Lovastatin. Lovastatin acid inhibits HMG-CoA reductase. This enzyme catalyzes the conversion of HMG-CoA to mevalonate, which is an early and rate limiting step in the biosynthesis of cholesterol. Lovastatin has been shown to reduce both normal and elevated low-density lipoprotein cholesterol (LDL-C). Lovastatin in approved for prevention of cardiovascular events and hypercholesterolemia. Off-label use of lovastatin includes treatmetn of diabetic dyslipidemia, familial dysbetalipoproteinemia, familial combined hyperlipidemia, or nephrotic hyperlipidemia. Lovastatin was tested in clinical trials agains radioation injury during therapy of prostate cancer.
Status:
US Approved Rx
(2010)
Source:
ANDA090339
(2010)
Source URL:
First approved in 1986
Source:
NDA050608
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Targets:
Conditions:
Sulbactam is a β-lactamase inhibitor given in combination with β-lactam antibiotics to inhibit β-lactamase, an enzyme produced by bacteria that destroys the antibiotics. Sulbactam in combination with semisynthetic antibiotic ampicillin sodium is indicated for the treatment of infections due to susceptible strains of the designated microorganisms: Skin and Skin Structure Infections caused by beta-lactamase producing strains of Staphylococcus aureus, Escherichia coli etc; Intra-Abdominal Infections caused by beta-lactamase producing strains of Escherichia coli, Klebsiella spp. (including K. Pneumoniae) tec; Gynecological Infections caused by beta-lactamase producing strains of Escherichia coli, and Bacteroides spp. (including B. fragilis).
Status:
US Approved Rx
(2022)
Source:
ANDA214172
(2022)
Source URL:
First approved in 1986
Source:
NDA019386
Source URL:
Class (Stereo):
CHEMICAL (RACEMIC)
Esmolol (trade name Brevibloc) is a cardioselective beta1 receptor blocker with rapid onset, a very short duration of action, and no significant intrinsic sympathomimetic or membrane stabilizing activity at therapeutic dosages. Esmolol decreases the force and rate of heart contractions by blocking beta-adrenergic receptors of the sympathetic nervous system, which are found in the heart and other organs of the body. Esmolol prevents the action of two naturally occurring substances: epinephrine and norepinephrine. Esmolol predominantly blocks the beta-1 receptors in cardiac tissue. Used for the rapid control of ventricular rate in patients with atrial fibrillation or atrial flutter in perioperative, postoperative, or other emergent circumstances where short term control of ventricular rate with a short-acting agent is desirable. Also used in noncompensatory sinus tachycardia where the rapid heart rate requires specific intervention.
Status:
US Approved Rx
(2021)
Source:
ANDA212533
(2021)
Source URL:
First approved in 1985
Source:
NDA018948
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Targets:
Conditions:
Levocarnitine propionate or Propionyl L-carnitine (PLC) is the propionyl ester of L-carnitine. Propionyl-L-carnitine stimulates energy production in ischaemic muscles by increasing citric acid cycle flux and stimulating pyruvate dehydrogenase activity. The free radical scavenging activity of the drug may also be beneficial. Propionyl-L-carnitine improves coagulative fibrinolytic homeostasis in vasal endothelium and positively affects blood viscosity. It exhibits a high affinity for the muscle enzyme, carnitine acyl transferase, and as such readily converts into propionyl-CoA and free carnitine. Most studies of the therapeutic use of PLC are focused on the prevention and treatment of ischemic heart disease, congestive heart failure, hypertrophic heart disease, and peripheral arterial disease. PLC is marketed under the trade name Dromos®. It is indicated for patients with peripheral arterial occlusive disorders and for exercise intolerance enhancement in patients with chronic congestive heart failure. Dromos is marketed in Italy.
Status:
US Approved Rx
(1998)
Source:
ANDA075028
(1998)
Source URL:
First approved in 1984
Source:
TRENTAL by VALIDUS PHARMS
Source URL:
Class (Stereo):
CHEMICAL (ACHIRAL)
Conditions:
Pentoxil (Pentoxifylline Extended-release Tablets, USP) is indicated for the treatment of patients with intermittent claudication based on chronic occlusive arterial disease of the limbs. Pentoxil can improve function and symptoms but is not intended to replace more definitive therapy, such as surgical bypass, or removal of arterial obstructions when treating peripheral vascular disease. Pentoxifylline and its metabolites improve the flow properties of blood by decreasing its viscosity. In patients with chronic peripheral arterial disease, this increases blood flow to the affected microcirculation and enhances tissue oxygenation. The precise mode of action of pentoxifylline and the sequence of events leading to clinical improvement are still to be defined. Pentoxifylline inhibits erythrocyte phosphodiesterase, resulting in an increase in erythrocyte cAMP activity. Subsequently, the erythrocyte membrane becomes more resistant to deformity. Along with erythrocyte activity, pentoxifylline also decreases blood viscosity by reducing plasma fibrinogen concentrations and increasing fibrinolytic activity. It is also a non-selective adenosine receptor antagonist. Pentoxifylline administration has been shown to produce dose-related hemorrheologic effects, lowering blood viscosity, and improving erythrocyte flexibility. Pentoxifylline has been shown to increase leukocyte deformability and to inhibit neutrophil adhesion and activation. Tissue oxygen levels have been shown to be significantly increased by therapeutic doses of pentoxifylline in patients with peripheral arterial disease. Clinical trials were conducted using either extended-release pentoxifylline tablets for up to 60 weeks or immediate-release pentoxifylline capsules for up to 24 weeks. Dosage ranges in the tablet studies were 400 mg bid to tid and in the capsule studies, 200-400 mg tid. The incidence of adverse reactions was higher in the capsule studies (where dose related increases were seen in digestive and nervous system side effects) than in the tablet studies. Studies with the capsule include domestic experience, whereas studies with the extended-release tablets were conducted outside the U.S.
Status:
US Approved Rx
(2024)
Source:
NDA216483
(2024)
Source URL:
First approved in 1984
Source:
COACTIN by ROCHE
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Targets:
Conditions:
Amdinocillin is a novel, semisynthetic penicillin effective against many gram-negative bacteria. The antibacterial activity of amdinocillin is derived from its ability to bind specifically and avidly to Penicillin Binding Protein-2 (PBP 2). Amdinocillin is active alone against many gram-negative organisms. Pseudomonas and non-fermenting gram-negative bacteria, however, are usually resistant. Amdinocillin, in combination with many beta-lactams, exhibits marked synergy against many enterobacteriaceae. No such synergy can be demonstrated for gram-positive organisms or pseudomonas species. Amdinocillin is not beta-lactamase stable. Organisms which produce high levels of plasma-mediated beta-lactamase are resistant to the drug. Used in the treatment of urinary tract infections caused by some strains of E. coli and klebsiella and enterobacter species. Used mainly against Gram negative organisms. Amdinocillin is not available in the United States.