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Status:
US Approved Rx
(2023)
Source:
NDA216974
(2023)
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
(2017)
Source:
ANDA206713
(2017)
Source URL:
First approved in 1986
Source:
CYKLOKAPRON by PHARMACIA AND UPJOHN
Source URL:
Class (Stereo):
CHEMICAL (ACHIRAL)
Targets:
Conditions:
Tranexamic acid is an antifibrinolytic that competitively inhibits the activation of plasminogen to plasmin. Tranexamic acid is a competitive inhibitor of plasminogen activation, and at much higher concentrations, a noncompetitive inhibitor of plasmin, i.e., actions similar to aminocaproic acid. Tranexamic acid is about 10 times more potent in vitro than aminocaproic acid. Tranexamic acid binds more strongly than aminocaproic acid to both the strong and weak receptor sites of the plasminogen molecule in a ratio corresponding to the difference in potency between the compounds. Tranexamic acid in a concentration of 1 mg per mL does not aggregate platelets in vitro. In patients with hereditary angioedema, inhibition of the formation and activity of plasmin by tranexamic acid may prevent attacks of angioedema by decreasing plasmin-induced activation of the first complement protein (C1). Tranexamic acid is used for use in patients with hemophilia for short term use (two to eight days) to reduce or prevent hemorrhage and reduce the need for replacement therapy during and following tooth extraction. It can also be used for excessive bleeding in menstruation, surgery, or trauma cases.
Status:
US Approved Rx
(1986)
Source:
NDA019353
(1986)
Source URL:
First approved in 1986
Source:
NDA019353
Source URL:
Class (Stereo):
CHEMICAL (ACHIRAL)
Targets:
Conditions:
Alfentanil is an opioid analgesic with a rapid onset of action. Alfentanil interacts predominately with the opioid mu-receptor. These mu-binding sites are discretely distributed in the human brain, spinal cord, and other tissues. In clinical settings, alfentanil exerts its principal pharmacologic effects on the central nervous system. Its primary actions of therapeutic value are analgesia and sedation. Alfentanil may increase the patient's tolerance for pain and decrease the perception of suffering, although the presence of the pain itself may still be recognized. In addition to analgesia, alterations in mood, euphoria and dysphoria, and drowsiness commonly occur. Alfentanil depresses the respiratory centers, depresses the cough reflex, and constricts the pupils. Alfentanil, marketed under the trade name Alfenta, Rapifen in Australia is indicated for the management of postoperative pain and the maintenance of general anesthesia.
Status:
US Approved Rx
(2003)
Source:
ANDA076025
(2003)
Source URL:
First approved in 1986
Source:
ATROVENT by BOEHRINGER INGELHEIM
Source URL:
Class (Stereo):
CHEMICAL (RACEMIC)
Targets:
Conditions:
Ipratropium (ipratropium bromide, ATROVENT® HFA) is a muscarinic antagonist structurally related to atropine but often considered safer and more effective for inhalation use. It is indicated for the maintenance treatment of bronchospasm associated with chronic obstructive pulmonary disease (COPD), including chronic bronchitis and emphysema. Ipratropium (ipratropium bromide, ATROVENT® HFA) is an anticholinergic (parasympatholytic) agent which, based on animal studies, appears to inhibit vagally-mediated reflexes by antagonizing the action of acetylcholine, the transmitter agent released at the neuromuscular junctions in the lung. Anticholinergics prevent the increases in intracellular concentration of Ca2+ which is caused by interaction of acetylcholine with the muscarinic receptors on bronchial smooth muscle.
Status:
US Approved Rx
(1986)
Source:
NDA018961
(1986)
Source URL:
First approved in 1986
Source:
NDA018961
Source URL:
Class (Stereo):
CHEMICAL (ACHIRAL)
Conditions:
Chromium sulfate(III) hexahydrate or chromium sulphate, a trivalent compound of chromium that was investigated as a toxic compound. Experiments on rodent have shown chromium sulfate produced severe and widespread effects in the nasal cavity, larynx, lungs, and mediastinal lymph node. Effects were characterized by the accumulation of foreign material, infiltration of alveolar macrophages, septal cell hyperplasia, and granulomatous and chronic inflammation. Besides, chromium sulphate exerted a disadvantageous effect on the skeleton, as it decreases bone density and resistance.
Status:
US Approved Rx
(1986)
Source:
NDA019193
(1986)
Source URL:
First approved in 1986
Source:
NDA019193
Source URL:
Class (Stereo):
CHEMICAL (RACEMIC)
Conditions:
Methacholine (trade name Provocholine) is a synthetic choline ester that acts as a muscarinic receptor agonist. Methacholine is primarily used to diagnose bronchial hyperreactivity, which is the hallmark of asthma and also occurs in chronic obstructive pulmonary disease. This is accomplished through the bronchial challenge test, or methacholine challenge, in which a subject inhales aerosolized methacholine, leading to bronchoconstriction.
Status:
US Approved Rx
(1993)
Source:
ANDA074014
(1993)
Source URL:
First approved in 1986
Source:
ORUDIS by WYETH AYERST
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Targets:
Conditions:
Dexketoprofen is a nonsteroidal anti-inflammatory drug (NSAID), manufactured by Menarini under the tradename Keral. Dexketoprofen is indicated for short-term treatment of mild to moderate pain, including dysmenorrhoea. Dexketoprofen works by blocking the action of a substance in the body called cyclo-oxygenase, which is involved in the production of chemicals in the body called prostaglandins. Prostaglandins are produced in response to injury or certain diseases and would otherwise go on to cause swelling, inflammation, and pain. By blocking cyclo-oxygenase, dexketoprofen prevents the production of prostaglandins and therefore reduces inflammation and pain. Along with peripheral analgesic action, it possesses central analgesic action. Dexketoprofen may cause dizziness, and patients should not, therefore, drive or operate heavy machinery or vehicles until they are familiar with how dexketoprofen affects them. Concomitant use of alcohol and other sedatives may potentiate this effect. In a small subset of individuals, the dizziness may be intolerable and require the transition to an alternative treatment.
Status:
US Approved Rx
(2015)
Source:
ANDA202087
(2015)
Source URL:
First approved in 1986
Source:
BUSPAR by BRISTOL MYERS SQUIBB
Source URL:
Class (Stereo):
CHEMICAL (ACHIRAL)
Conditions:
Buspirone is the first of a new class of anxioselective agents, the azaspirodecanediones. Animal studies have suggested antianxiety activity and the absence of abuse potential. Behavioural, electrophysiological and receptor binding experiments gradually led to the idea that buspirone owes much of its anxiolytic activity to its ability to attenuate central 5-hydroxytryptamine neurotransmission. In vitro preclinical studies have shown that buspirone has a high affinity for serotonin (5-HT1A) receptors. Some studies do suggest that buspirone may have indirect effects on other neurotransmitter systems. Buspirone differs from typical benzodiazepine anxiolytics in that it does not exert anticonvulsant or muscle relaxant effects. It also lacks the prominent sedative effect that is associated with more typical anxiolytics. The drug was approved by FDA for the treatment of anxiety.
Status:
US Approved Rx
(2023)
Source:
ANDA218181
(2023)
Source URL:
First approved in 1986
Source:
PEPCID by BAUSCH
Source URL:
Class (Stereo):
CHEMICAL (ACHIRAL)
Famotidine, a competitive histamine H2-receptor antagonist, is used to treat gastrointestinal disorders such as gastric or duodenal ulcer, gastroesophageal reflux disease, and pathological hypersecretory conditions. Famotidine inhibits many of the isoenzymes of the hepatic CYP450 enzyme system. Other actions of Famotidine include an increase in gastric bacterial flora such as nitrate-reducing organisms. Famotidine binds competitively to H2-receptors located on the basolateral membrane of the parietal cell, blocking histamine affects. This competitive inhibition results in reduced basal and nocturnal gastric acid secretion and a reduction in gastric volume, acidity, and amount of gastric acid released in response to stimuli including food, caffeine, insulin, betazole, or pentagastrin.
Status:
US Approved Rx
(2013)
Source:
NDA202091
(2013)
Source URL:
First approved in 1986
Source:
ANDA065355
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Cefixime, an antibiotic, is a third-generation cephalosporin like ceftriaxone and cefotaxime. Cefixime is highly stable in the presence of beta-lactamase enzymes. As a result, many organisms resistant to penicillins and some cephalosporins due to the presence of beta-lactamases, may be susceptible to cefixime. The antibacterial effect of cefixime results from inhibition of mucopeptide synthesis in the bacterial cell wall. Like all beta-lactam antibiotics, cefixime binds to specific penicillin-binding proteins (PBPs) located inside the bacterial cell wall, causing the inhibition of the third and last stage of bacterial cell wall synthesis. Cell lysis is then mediated by bacterial cell wall autolytic enzymes such as autolysins; it is possible that cefixime interferes with an autolysin inhibitor. Cefixime is sold under the brand name Suprax, indicated for the treatment of:
Uncomplicated Urinary Tract Infections
Otitis Media
Pharyngitis and Tonsillitis
Acute Exacerbations of Chronic Bronchitis
Uncomplicated Gonorrhea (cervical/urethral)