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Restrict the search for
beta carotene
to a specific field?
Status:
US Approved Rx
(1978)
Source:
NDA050514
(1978)
Source URL:
First approved in 1978
Source:
NDA050514
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Targets:
Natamycin (Pimaricin, Pimafucin, Natadrops, Natacyn) is a polyene antifungal agent originally isolated from Streptomyces natalensis found in a soil sample from Natal, South Africa. Natamycin was discovered in DSM laboratories in 1955. Similar to other polyenes, natamycin binds to ergosterol in the fungal cell membrane. Natamycin blocks fungal growth by binding specifically to ergosterol with¬out permeabilizing the membrane where it inhibits vacuole fusion at the priming phase and interferes with membrane protein functions. Natamycin is also used in the food industry as an effective preservative. Natamycin is active against most Candida spp. Aspergillus spp., Fusarium spp. and other rarer fungi that cause keratitis. Secondary or acquired resistance is probably rare, but not extensively studied. Natamycin is not effective in vitro against gram-positive or gram-negative bacteria. Topical administration appears to produce effective concentrations of natamycin within the corneal stroma but not in intraocular fluid. Natamycin is poorly soluble in water and not absorbed through the skin or mucous membranes, including the vagina. Very little is absorbed through the gastrointestinal tract. After ocular application, therapeutic concentrations are present within the infected cornea, but not in intra-ocular fluid Natamycin may cause some irritation on skin or mucous membranes
Status:
US Approved Rx
(2017)
Source:
ANDA207440
(2017)
Source URL:
First approved in 1977
Source:
FLORONE by PFIZER
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Targets:
Conditions:
Diflorasone is a topical corticosteroid used to treat itching and inflammation of the skin. Topical corticosteroids share anti-inflammatory, antipruritic and vasoconstrictive actions. The mechanism of anti-inflammatory activity of the topical corticosteroids is unclear. Various laboratory methods, including vasoconstrictor assays, are used to compare and predict potencies and/or clinical efficacies of the topical corticosteroids. There is some evidence to suggest that a recognizable correlation exists between vasoconstrictor potency and therapeutic efficacy in man. The extent of percutaneous absorption of topical corticosteroids is determined by many factors including the vehicle, the integrity of the epidermal barrier, and the use of occlusive dressings. Topical corticosteroids can be absorbed from normal intact skin. Inflammation and/or other disease processes in the skin increase percutaneous absorption. Occlusive dressings substantially increase the percutaneous absorption of topical corticosteroids. Thus, occlusive dressings may be a valuable therapeutic adjunct for treatment of resistant dermatoses. Once absorbed through the skin, topical corticosteroids are handled through pharmacokinetic pathways similar to systemically administered corticosteroids. Corticosteroids are bound to plasma proteins in varying degrees. They are metabolized primarily in the liver and are then excreted by the kidneys. Some of the topical corticosteroids and their metabolites are also excreted into the bile.
Status:
US Approved Rx
(2005)
Source:
NDA021807
(2005)
Source URL:
First approved in 1977
Source:
NOLVADEX by ASTRAZENECA
Source URL:
Class (Stereo):
CHEMICAL (ACHIRAL)
Tamoxifen (brand name Nolvadex), is selective estrogen receptor modulators (SERM) with tissue-specific activities for the treatment and prevention of estrogen receptor positive breast cancer. Tamoxifen itself is a prodrug, having relatively little affinity for its target protein, the estrogen receptor (ER). It is metabolized in the liver by the cytochrome P450 isoform CYP2D6 and CYP3A4 into active metabolites such as 4-hydroxytamoxifen (4-OHT) (afimoxifene) and N-desmethyl-4-hydroxytamoxifen (endoxifen) which have 30–100 times more affinity with the ER than tamoxifen itself. These active metabolites compete with estrogen in the body for binding to the ER. In breast tissue, 4-OHT acts as an ER antagonist so that transcription of estrogen-responsive genes is inhibited. Tamoxifen has 7% and 6% of the affinity of estradiol for the ERα and ERβ, respectively, whereas 4-OHT has 178% and 338% of the affinity of estradiol for the ERα and ERβ. The prolonged binding of tamoxifen to the nuclear chromatin of these results in reduced DNA polymerase activity, impaired thymidine utilization, blockade of estradiol uptake, and decreased estrogen response. It is likely that tamoxifen interacts with other coactivators or corepressors in the tissue and binds with different estrogen receptors, ER-alpha or ER-beta, producing both estrogenic and antiestrogenic effects. Tamoxifen is currently used for the treatment of both early and advanced estrogen receptor (ER)-positive (ER+) breast cancer in pre- and post-menopausal women. Additionally, it is the most common hormone treatment for male breast cancer. Patients with variant forms of the gene CYP2D6 (also called simply 2D6) may not receive full benefit from tamoxifen because of too slow metabolism of the tamoxifen prodrug into its active metabolites. Tamoxifen is used as a research tool to trigger tissue-specific gene expression in many conditional expression constructs in genetically modified animals including a version of the Cre-Lox recombination technique. Tamoxifen has been shown to be effective in the treatment of mania in patients with bipolar disorder by blocking protein kinase C (PKC), an enzyme that regulates neuron activity in the brain. Researchers believe PKC is over-active during the mania in bipolar patients.
Status:
US Approved Rx
(2007)
Source:
ANDA077088
(2007)
Source URL:
First approved in 1977
Source:
LIORESAL by NOVARTIS
Source URL:
Class (Stereo):
CHEMICAL (RACEMIC)
Targets:
Conditions:
Baclofen (brand names Kemstro, Lioresal, and Gablofen) is a derivative of gamma-aminobutyric acid (GABA). Baclofen is a muscle relaxer and an antispastic agent and is used to treat muscle symptoms caused by multiple sclerosis, including spasm, pain, and stiffness. It is primarily used to treat spasticity and is under investigation for the treatment of alcoholism. Although baclofen is an analog of the putative inhibitory neurotransmitter gamma-aminobutyric acid (GABA), there is no conclusive evidence that actions on GABA systems are involved in the production of its clinical effects. Baclofen is rapidly and extensively absorbed and eliminated. Absorption may be dose-dependent, being reduced with increasing doses. Baclofen is excreted primarily by the kidney in unchanged form and there is relatively large intersubjective variation in absorption and/or elimination. Baclofen is a direct agonist at GABA-B receptors. The precise mechanism of action of baclofen is not fully known. It is capable of inhibiting both monosynaptic and polysynaptic reflexes at the spinal level, possibly by hyperpolarization of afferent terminals, although actions at supraspinal sites may also occur and contribute to its clinical effect.
Status:
US Approved Rx
(2020)
Source:
ANDA209595
(2020)
Source URL:
First approved in 1977
Source:
TOPICORT by TARO
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Targets:
Conditions:
Desoximetasone (Topicort®) is a topical anti-inflammatory glucocorticoid indicated for the relief of the inflammatory and pruritic manifestations of corticosteroid-responsive dermatoses and for the treatment of plaque psoriasis in patients 18 years of age or older. The topical corticosteroids constitute a class of primarily synthetic steroids used as anti-inflammatory and antipruritic agents. They play a role in cellular signaling, immune function, inflammation and protein regulation; however, the precise mechanism of action in psoriasis is unknown. The mechanism of anti-inflammatory activity of the topical corticosteroids is also unclear. Various laboratory methods, including vasoconstrictor assays, are used to compare and predict potencies and/or clinical efficacies of the topical corticosteroids. There is some evidence to suggest that a recognizable correlation exists between vasoconstrictor potency and therapeutic efficacy in man.
Status:
US Approved Rx
(1977)
Source:
NDA017765
(1977)
Source URL:
First approved in 1977
Source:
NDA017765
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Conditions:
Clocortolone (used in form of pivalate prodrug) is a topical glucocorticoid that was approved by FDA for the treatment of corticosteroid-responsive skin disorders. The drug exerts its anti-inflammatory action by binding to glucocorticoid receptor which results in regulation of the expression of proinflammatory cytokines and further antiproliferative, immunosuppressive, and initial vasoconstrictive effects.
Status:
US Approved Rx
(2012)
Source:
NDA202813
(2012)
Source URL:
First approved in 1976
Source:
VANCERIL by SCHERING
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Status:
US Approved Rx
(2005)
Source:
ANDA077133
(2005)
Source URL:
First approved in 1976
Source:
VIRA-A by PARKEDALE
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Conditions:
Adenosine is a nucleoside that is composed of adenine and d-ribose, occurring in all cells of the body and play many important biological roles in addition to being components of DNA and RNA. Adenosine itself is a neurotransmitter. Adenocard (adenosine injection) is used as an initial treatment for the termination of paroxysmal supraventricular tachycardia (PVST), including that associated with accessory bypass tracts (Wolff-Parkinson-White Syndrome). When clinically advisable, appropriate vagal maneuvers. Adenocard does not convert atrial flutter, atrial fibrillation, or ventricular tachycardia to normal sinus rhythm. In the presence of atrial flutter or atrial fibrillation, a transient modest slowing of ventricular response may occur immediately following Adenocard administration. Adenosine slows conduction time through the A-V node, can interrupt the reentry pathways through the A-V node, and can restore normal sinus rhythm. This effect may be mediated through the drug's activation of cell-surface A1 and A2 adenosine receptors. Adenocard is antagonized competitively by methylxanthines such as caffeine and theophylline, and potentiated by blockers of nucleoside transport such as dipyridamole. Adenocard is not blocked by atropine. Adenosine also inhibits the slow inward calcium current and activation of adenylate cyclase in smooth muscle cells, thereby causing relaxation of vascular smooth muscle. By increasing blood flow in normal coronary arteries with little or no increase in stenotic arteries, adenosine produces a relative difference in thallous (thallium) chloride TI 201 uptake in myocardium supplied by normal verus stenotic coronary arteries.
Status:
US Approved Rx
(2019)
Source:
ANDA211033
(2019)
Source URL:
First approved in 1975
Source:
NDA017533
Source URL:
Class (Stereo):
CHEMICAL (ACHIRAL)
Targets:
Conditions:
Clonazepam, a benzodiazepine, is used primarily as an anticonvulsant in the treatment of absence seizures, petit mal variant seizures (Lennox-Gastaut syndrome), akinetic and myoclonic seizures, and nocturnal myoclonus. Klonopin is the brand name for Clonazepam, an anxiolytic and anticonvulsant. The precise mechanism by which clonazepam exerts its antiseizure
and antipanic effects is unknown, although it is believed to be related to its ability to
enhance the activity of gamma aminobutyric acid (GABA), the major inhibitory
neurotransmitter in the central nervous system. Allosteric interactions between central benzodiazepine receptors and gamma-aminobutyric acid (GABA) receptors potentiate the effects of GABA. As GABA is an inhibitory neurotransmitter, this results in increased inhibition of the ascending reticular activating system. Benzodiazepines, in this way, block the cortical and limbic arousal that occurs following stimulation of the reticular pathways.
Status:
US Approved Rx
(1974)
Source:
NDA017556
(1974)
Source URL:
First approved in 1974
Source:
NDA017556
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Targets:
Halcinonide is one of the available highly potent topical cor¬ticosteroids. It is a derivative of hydrocortisone and contains important modifications in its structure that alter its absorption, potency, and adverse effects compared with hydrocortisone. Halcinonide—along with desoximetasone, betamethasone, fluocinonide, and diflorasone diacetate—is classified as a Class II potency corticosteroid. Although similar in strength, halcinonide in Halog (the only topical product available that contains halcinonide) differs from many other compounds of this class in the formulation. Halcinonide cream is formulated in a biphasic base that allows for immediate-release of halcinonide upon application to the skin, followed by a delayed and sustained release of halcinonide over time. This “dual formulation” strategy allows for prolonged halcinonide activity. The formulation of halcinonide cream contains microcrystals of halcinonide. An equilibrium is established between dissolved halcinonide in the cream and non-dissolved halcinonide in the microcrystals. As soluble hal¬cinonide enters the skin, additional quantities of halcinonide from the microcrystals become available as a new equilibrium is established. This dynamic equilibrium serves to maintain a sustained level of halcinonide well beyond the time of application.
