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Restrict the search for
amphotericin b
to a specific field?
Status:
US Approved Rx
(2016)
Source:
ANDA202674
(2016)
Source URL:
First approved in 1997
Source:
NDA020639
Source URL:
Class (Stereo):
CHEMICAL (ACHIRAL)
Quetiapine, marketed as SEROQUEL XR, is an atypical antipsychotic approved for the treatment of schizophrenia, bipolar disorder, and along with an antidepressant to treat major depressive disorder. The mechanism of action of SEROQUEL XR in the treatment of schizophrenia, bipolar disorder and major depressive disorder (MDD), is unknown. However, its efficacy in schizophrenia could be mediated through a combination of dopamine type 2 (D2) and serotonin type 2A (5HT2A) antagonism. The active metabolite, N-desalkyl quetiapine (norquetiapine), has similar activity at D2, but greater activity at 5HT2A receptors, than the parent drug (quetiapine). Quetiapine’s efficacy in bipolar depression and MDD may partly be explained by the high affinity and potent inhibitory effects that norquetiapine exhibits for the norepinephrine transporter. Antagonism at receptors other than dopamine and serotonin with similar or greater affinities may explain some of the other effects of quetiapine and norquetiapine: antagonism at histamine H1 receptors may explain the somnolence, antagonism at adrenergic α1b receptors may explain the orthostatic hypotension, and antagonism at muscarinic M1 receptors may explain the anticholinergic effects. Quetiapine and norquetiapine have affinity for multiple neurotransmitter receptors including dopamine D1 and D2, serotonin 5HT1A and 5HT2A, histamine H1, muscarinic M1, and adrenergic α1b and α2 receptors. Quetiapine differs from norquetiapine in having no appreciable affinity for muscarinic M1 receptors whereas norquetiapine has high affinity. Quetiapine and norquetiapine lack appreciable affinity for benzodiazepine receptors.
Status:
US Approved Rx
(2018)
Source:
NDA210867
(2018)
Source URL:
First approved in 1997
Source:
NADA141087
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Conditions:
Moxidectin is a semi-synthetic methoxime derivative of LL F-2924α, commonly referred as F-alpha or nemadectin F-alpha is a product of fermentation of Streptomyces cyaneogriseus subsp. noncyanogenus, a bacterial organism isolated in 1983 from a sample of sand from Victoria, Australia. Moxidectin is a potent, broad-spectrum endectocide with activity against a wide range of nematodes, insects and acari. The compound acts by binding to ligand-gated chloride channels, more specifically the subtypes that are gamma-aminobutyric (GABA) mediated and glutamate-gated. The consequence of Moxidectin binding and activation is an increased permeability, leading to an influx of chloride ions and flaccid paralysis of the parasite leading to death. The macrocyclic lactones probably act by binding to and opening glutamate-gated chloride channels found only in neurons and myocytes of invertebrates. Because moxidectin is very lipophilic, it becomes highly concentrated in the serum. When the concentration of moxidectin in the serum is high, moxidectin is able to cross the blood-brain barrier. Once it is in the central nervous system, a macrocyclic lactone stimulates the synaptic secretion of the inhibitory neurotransmitter, GABA. By binding at the receptor site, GABA causes influx of chloride ions into neurons, causing the neurons to become hyperpolarised, which in turn, causes diminution in neuronal activity, resulting in sedation and relaxation of the skeletal muscles. Signs displayed by foals with moxidectin toxicity included dyspnoea, depression, ataxia, weakness, coma and seizures. In a Phase 3 study compared the efficacy, safety and tolerability of moxidectin and ivermectin in subjects infected with Onchocerca volvulus, which is the parasite that causes river blindness.
Status:
US Approved Rx
(2023)
Source:
ANDA207209
(2023)
Source URL:
First approved in 1997
Source:
PRANDIN by GEMINI LABS LLC
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Targets:
Conditions:
Repaglinide is antidiabetic drug, which is sold under several names including, Prandin in the U.S., Surepost in Japan and GlucoNorm in Canada. It is an oral blood glucose-lowering drug of the meglitinide class used in the management of type 2 diabetes mellitus (also known as non-insulin dependent diabetes mellitus or NIDDM). Repaglinide lowers blood glucose levels by stimulating the release of insulin from the pancreas. This action is dependent upon functioning beta (ß) cells in the pancreatic islets. Insulin secretion by pancreatic β cells is partly controlled by cellular membrane potential. Membrane potential is regulated through an inverse relationship between the activity of cell membrane ATP-sensitive potassium channels (ABCC8) and extracellular glucose concentrations. Extracellular glucose enters the cell via GLUT2 (SLC2A2) transporters. Once inside the cell, glucose is metabolized to produce ATP. High concentrations of ATP inhibit ATP-sensitive potassium channels causing membrane depolarization. High glucose concentrations cause ATP-sensitive potassium channels to close resulting in membrane depolarization and opening of L-type calcium channels. The influx of calcium ions stimulates calcium-dependent exocytosis of insulin granules. Repaglinide closes ATP-dependent potassium channels in the ß-cell membrane by binding at characterizable sites. This potassium channel blockade depolarizes the ß-cell, which leads to an opening of calcium channels. The resulting increased calcium influx induces insulin secretion. The ion channel mechanism is highly tissue selective with low affinity for heart and skeletal muscle. Repaglinide is completely metabolized by oxidative biotransformation and direct conjugation with glucuronic acid after either an IV or oral dose.
Status:
US Approved Rx
(2016)
Source:
ANDA205074
(2016)
Source URL:
First approved in 1997
Source:
ZOMIG by IPR
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Conditions:
Zolmitriptan (Zomig; formerly 311C90) is a novel 5-hydroxytryptamine (5HT)1B/1D receptor agonist with proven efficacy in the acute treatment of migraine with or without preceding aura. The N-desmethyl metabolite also has high affinity for 5-HT1B/1D and moderate affinity for 5-HT1A receptors. Migraines are likely due to local cranial vasodilatation and/or to the release of sensory neuropeptides (vasoactive intestinal peptide, substance P and calcitonin gene-related peptide) through nerve endings in the trigeminal system. The therapeutic activity of Zomig for the treatment of migraine headache is thought to be due to the agonist effects at the 5-HT1B/1D receptors on intracranial blood vessels (including the arterio-venous anastomoses) and sensory nerves of the trigeminal system, which result in cranial vessel constriction, and inhibition of pro-inflammatory neuropeptide release.
Status:
US Approved Rx
(2005)
Source:
ANDA076468
(2005)
Source URL:
First approved in 1997
Source:
NDA020333
Source URL:
Class (Stereo):
CHEMICAL (ACHIRAL)
Conditions:
Anagrelide is an orally active quinazinolone derivative that was originally developed as an antiplatelet drug. The drug inhibits cyclic nucleotide phosphodiesterase III (PDEIII) and phopholipase A2, which is thought to cause the side effects of vasodilation, positive inotropism, reduced platelet aggregation. However, significant inhibition of platelet aggregation is observed only at doses of anagrelide higher than those required to reduce platelet count. It is indicated for the treatment of patients with thrombocythemia, secondary to myeloproliferative disorders. Commonly reported side effects of anagrelide include: abdominal pain, dizziness, headache, nausea, and palpitations. Other side effects include: back pain, fever, tachycardia, vomiting, and anorexia. There is a single case report, which suggests that sucralfate may interfere with anagrelide absorption. Anagrelide is an inhibitor of cyclic AMP PDE III. The effects of medicinal products with similar properties such as inotropes milrinone, enoximone, amrinone, olprinone and cilostazol may be exacerbated by anagrelide.
Status:
US Approved Rx
(2011)
Source:
ANDA090289
(2011)
Source URL:
First approved in 1997
Source:
NDA020726
Source URL:
Class (Stereo):
CHEMICAL (ACHIRAL)
Targets:
Conditions:
Letrozole (trade name Femara), a nonsteroidal aromatase inhibitor. Femara is indicated for the adjuvant treatment of postmenopausal women with hormone receptor positive early breast cancer. Also is indicated for the extended adjuvant treatment of early breast cancer in postmenopausal women, who have received 5 years of adjuvant tamoxifen therapy. Femara has to be used for first-line treatment of postmenopausal women with hormone receptor positive or unknown, locally advanced or metastatic breast cancer and for the treatment of advanced breast cancer in postmenopausal women with disease progression following antiestrogen therapy. Treatment of breast cancer thought to be hormonally responsive (i.e., estrogen and/or progesterone receptor positive or receptor unknown) has included a variety of efforts to decrease estrogen levels (ovariectomy, adrenalectomy, hypophysectomy) or inhibit estrogen effects (antiestrogens and progestational agents). These interventions lead to decreased tumor mass or delayed progression of tumor growth in some women. In postmenopausal women, estrogens are mainly derived from the action of the aromatase enzyme, which converts adrenal androgens (primarily androstenedione and testosterone) to estrone and estradiol. The suppression of estrogen biosynthesis in peripheral tissues and in the cancer tissue itself can therefore be achieved by specifically inhibiting the aromatase enzyme. Letrozole inhibits the conversion of androgens to estrogens. Letrozole selectively inhibits gonadal steroidogenesis but has no significant effect on adrenal mineralocorticoid or glucocorticoid synthesis. Letrozole inhibits the aromatase enzyme by competitively binding to the heme of the cytochrome P450 subunit of the enzyme, resulting in a reduction of estrogen biosynthesis in all tissues. Treatment of women with letrozole significantly lowers serum estrone, estradiol and estrone sulfate and has not been shown to significantly affect adrenal corticosteroid synthesis, aldosterone synthesis, or synthesis of thyroid hormones. Letrozole is rapidly and completely absorbed from the gastrointestinal tract and absorption is not affected by food. Metabolism to a pharmacologically inactive carbinol metabolite (4,4'¬ methanol-bisbenzonitrile) and renal excretion of the glucuronide conjugate of this metabolite is the major pathway of letrozole clearance. In human microsomes with specific CYP isozyme activity, CYP3A4 metabolized letrozole to the carbinol metabolite while CYP2A6 formed both this metabolite and its ketone analog. In human liver microsomes, letrozole strongly inhibited CYP2A6 and moderately inhibited CYP2C19. The most common side effects are sweating, hot flashes, arthralgia (joint pain), and fatigue
Status:
US Approved Rx
(2023)
Source:
ANDA206027
(2023)
Source URL:
First approved in 1997
Source:
Duract
Source URL:
Class (Stereo):
CHEMICAL (ACHIRAL)
Conditions:
Bromfenac is a topical, nonsteroidal anti-inflammatory drug (NSAID) for ophthalmic use. It is indicated for the treatment of postoperative inflammation and reduction of ocular pain in patients who have undergone cataract surgery. The mechanism of its action is thought to be due to its ability to block prostaglandin synthesis by inhibiting cyclooxygenase 1 and 2. The most commonly reported adverse reactions in 3 to 8% of patients were anterior chamber inflammation, foreign body sensation, eye pain, photophobia and vision blurred.
Status:
US Approved Rx
(2022)
Source:
ANDA204928
(2022)
Source URL:
First approved in 1996
Source:
NDA020547
Source URL:
Class (Stereo):
CHEMICAL (ACHIRAL)
Conditions:
Zafirlukast is an oral leukotriene receptor antagonist (LTRA) for the maintenance treatment of asthma, often used in conjunction with an inhaled steroid and/or long-acting bronchodilator. It is available as a tablet and is usually dosed twice daily. Zafirlukast is indicated for the prophylaxis and chronic treatment of asthma. Patients with asthma were found in one study to be 25-100 times more sensitive to the bronchoconstricting activity of inhaled LTD4 than nonasthmatic subjects. In vitro studies demonstrated that zafirlukast antagonized the contractile activity of three leukotrienes (LTC4, LTD4 and LTE4) in conducting airway smooth muscle from laboratory animals and humans. Zafirlukast prevented intradermal LTD4-induced increases in cutaneous vascular permeability and inhibited inhaled LTD4-induced influx of eosinophils into animal lungs. Zafirlukast is a selective and competitive receptor antagonist of leukotriene D4 and E4 (LTD4 and LTE4), components of slow-reacting substance of anaphylaxis (SRSA). Cysteinyl leukotriene production and receptor occupation have been correlated with the pathophysiology of asthma, including airway edema, smooth muscle constriction, and altered cellular activity associated with the inflammatory process, which contribute to the signs and symptoms of asthma. Zafirlukast is marketed by Astra Zeneca with the brand names Accolate, Accoleit, and Vanticon. It was the first LTRA to be marketed in the USA and is now approved in over 60 countries, including the UK, Japan, Taiwan, Italy, Spain, Canada, Brazil, China and Turkey.
Status:
US Approved Rx
(2024)
Source:
ANDA217118
(2024)
Source URL:
First approved in 1996
Source:
NDA020702
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Targets:
Conditions:
Atorvastatin calcium (LIPITOR®) is a pyrrole and heptanoic acid derivative, a synthetic lipid-lowering agent. Atorvastatin is a selective, competitive inhibitor of 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase. This enzyme catalyzes the conversion of HMG-CoA to mevalonate, an early and rate-limiting step in cholesterol biosynthesis. Atorvastatin is used to reduce serum levels of LDL(low-density lipoprotein)-cholesterol; apolipoprotein B; and triglycerides and to increase serum levels of HDL(high-density lipoprotein)-cholesterol in the treatment of hyperlipidemias and prevention of cardiovascular disease in patients with multiple risk factors.
Status:
US Approved Rx
(2020)
Source:
ANDA210594
(2020)
Source URL:
First approved in 1996
Source:
NDA020630
Source URL:
Class (Stereo):
CHEMICAL (ACHIRAL)
Targets:
Conditions:
Remifentanil (marketed by Abbott as Ultiva) is a potent ultra short-acting synthetic opioid analgesic drug. It is given to patients during surgery to relieve pain and as an adjunct to an anaesthetic. ULTIVA is a µ-opioid agonist with rapid onset and peak effect, and short duration of action. The
µ-opioid activity of ULTIVA is antagonized by opioid antagonists such as naloxone. ULTIVA is indicated for IV administration:
1. As an analgesic agent for use during the induction and maintenance of general anesthesia for inpatient and outpatient procedures.
2. For continuation as an analgesic into the immediate postoperative period in adult patients under the direct supervision of an anesthesia practitioner in a postoperative anesthesia care unit or intensive care setting.
3. As an analgesic component of monitored anesthesia care in adult patients.
