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Restrict the search for
segesterone acetate
to a specific field?
Status:
US Previously Marketed
Source:
21 CFR 310.536(a) nailbiting or thumbsucking deterrent sucrose octaacetate
Source URL:
First approved in 2015
Source:
Benzalkonium Chloride, Benzyl Alcohol by Meridian Animal Health
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Conditions:
Sucrose octaacetate is an acetylated derivative of sucrose. It can be used as a bitter additive, a denaturant for alcohol, a soaker for paper, as well as an insecticide, plasticizer for cellulosic&synthetic resin. It also can be used as an additive for paint and children's toys, etc. It can prevent mice or children from biting or tasting the goods because of its extreme bitter taste. Sucrose octaacetate was determined by the EPA to be usable as an inert ingredient in pesticides due to its low toxicity
Status:
US Previously Marketed
Source:
ALTABAX by ALMIRALL
(2007)
Source URL:
First approved in 2007
Source:
ALTABAX by ALMIRALL
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Targets:
Retapamulin is a topical antibiotic which was approved by FDA (Altabax brand name) for the treatment of impetigo due to Staphylococcus aureus (methicillin-susceptible isolates only) or Streptococcus pyogenes. Retapamulin exerts its antibacterial action by binding to 50S subunit of the bacterial ribosome.
Status:
US Previously Marketed
Source:
RAPLON by ORGANON USA INC
(1999)
Source URL:
First approved in 1999
Source:
RAPLON by ORGANON USA INC
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Targets:
Conditions:
Rapacuronium bromide (RAPLON), a nondepolarizing neuromuscular blocking agent, is a negative allosteric modulator of muscarinic acetylcholine receptors. Rapacuronium bromide is indicated as an adjunct to general anesthesia to facilitate tracheal intubation and to provide skeletal muscle relaxation during surgical procedures. There were no specific pharmacokinetic studies conducted to examine the drug-drug interactions of RAPLON. Due to the risk of fatal bronchospasm, it was withdrawn from the United States market less than 2 years after its FDA approval.
Status:
US Previously Marketed
Source:
ORLAAM by ROXANE
(1993)
Source URL:
First approved in 1993
Source:
ORLAAM by ROXANE
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Status:
US Previously Marketed
Source:
DIDANOSINE by NORVIUM BIOSCIENCE
(2010)
Source URL:
First approved in 1991
Source:
VIDEX by BRISTOL MYERS SQUIBB
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Conditions:
Didanosine was developed by Bristol-Myers Squibb in collaboration with the NIH for the treatment of HIV-1 infections. Upon administration the drug is metabolized to the active metabolite which inhibits HIV-1 reverse transcriptase both by competing with deoxyadenosine 5'-triphosphate and by its incorporation into viral DNA. Didanosine was approved by FDA under the name Videx (among the other names).
Status:
First approved in 1990
Class (Stereo):
CHEMICAL (ABSOLUTE)
Status:
US Previously Marketed
Source:
METIPRANOLOL by SANDOZ
(2001)
Source URL:
First approved in 1989
Source:
OPTIPRANOLOL by BAUSCH AND LOMB
Source URL:
Class (Stereo):
CHEMICAL (RACEMIC)
Conditions:
Metipranolol is a beta-adrenergic antagonist effective for both beta-1 and beta-2 receptors. It is used as an antiarrhythmic, antihypertensive, and antiglaucoma agent. Metipranolol blocks beta1 and beta2 (non-selective) adrenergic receptors. It does not have significant intrinsic sympathomimetic activity, and has only weak local anesthetic (membrane-stabilizing) and myocardial depressant activity.
Orally administered beta-adrenergic blocking agents reduce cardiac output in both healthy subjects and patients with heart disease. In patients with severe impairment of myocardial function, beta-adrenergic receptor antagonists may inhibit the sympathetic stimulatory effect necessary to maintain adequate cardiac output. Metipranolol when applied topically in the eye, has the action of reducing elevated as well as normal intraocular pressure (IOP), whether or not accompanied by glaucoma. Elevated intraocular pressure is a major risk factor in the pathogenesis of glaucomatous visual field loss. The higher the level of intraocular pressure, the greater the likelihood of glaucomatous visual field loss and optic nerve damage.
The primary mechanism of the ocular hypotensive action of Metipranolol is most likely due to reduction in aqueous humor production. A slight increase in outflow may be an additional mechanism. Metipranolol reduces IOP with little or no effect on pupil size or accommodation. Metipranolol is known as the brand OptiPranolol. Brand-name OptiPranolol is manufactured by Bausch & Lomb Incorporated. However, the patents for OptiPranolol have expired, and this medication is currently available in generic form. Generic OptiPranolol eye drops are available in one strength -- metipranolol 0.3 percent solution. It is made by Falcon Pharmaceuticals.
Status:
US Previously Marketed
Source:
MAXAIR by BAUSCH
(1986)
Source URL:
First approved in 1986
Source:
MAXAIR by BAUSCH
Source URL:
Class (Stereo):
CHEMICAL (RACEMIC)
Targets:
Conditions:
Pirbuterol (trade name Maxair) is a short-acting β2 adrenoreceptor agonist with bronchodilating action used in the treatment of asthma. The pharmacologic effects of beta-adrenergic agonist drugs, including pirbuterol, are at least in proof attributable to stimulation through beta-adrenergic receptors of intracellular adenyl cyclase, the enzyme which catalyzes the conversion of adenosine triphosphate (ATP) to cyclic-adenosine monophosphate (c-AMP). Increased c-AMP levels are associated with relaxation of bronchial smooth muscle and inhibition of release of mediators of immediate hypersensitivity from cells, especially from mast cells. Pirbuterol is used in asthma for reversal of acute bronchospasm, and also as a maintenance medication to prevent future attacks. It should be used in patients 12 years of age and older with or without concurrent theophylline and/or inhaled corticosteroid. After inhalation of doses up to 800 μg (twice the maximum recommended dose) systemic blood levels of pirbuterol are below the limit of assay sensitivity (2–5 ng/ml). A mean of 51% of the dose is recovered in urine as pirbuterol plus its sulfate conjugate following administration by aerosol. Pirbuterol is not metabolized by catechol-O-methyltransferase.
Status:
US Previously Marketed
Source:
GUANABENZ ACETATE by CHARTWELL RX
(1998)
Source URL:
First approved in 1982
Source:
WYTENSIN by WYETH AYERST
Source URL:
Class (Stereo):
CHEMICAL (ACHIRAL)
Targets:
Conditions:
Guanabenz, an antihypertensive agent for oral administration-, is an aminoguanidine derivative, 2,'6-dichlorobenzylideneamina-guanidine acetate. It is white to an almost white powder having not more than a slight odor. Sparingly soluble in water and in 0.1 N hydrochloric acid; soluble in alcohol and in propylene glycol.
Guanabenz is an orally active central alpha-2 adrenergic agonist. Its antihypertensive action appears to be mediated via stimulation of central alpha-adrenergic receptors, resulting in a decrease of sympathetic outflow from the brain at the bulbar level to the peripheral circulatory system. In clinical trials, guanabenz acetate, given orally to hypertensive patients, effectively controlled blood pressure without any significant effect on glomerular filtration rate, renal blood flow, body fluid volume or body weight. The Myelin Repair Foundation and the National Institutes of Health (National Institute of Neurological Disorders and Stroke) are developing guanabenz for the treatment of multiple sclerosis. Unlike the currently available treatment for multiple sclerosis that suppresses the immune system, guanabenz, an FDA approved the drug for the treatment of high blood pressure, has a potential to reduce the loss of myelin by protecting and repairing myelin-producing cells in the brain from damage. Phase I development is underway in the US.
Status:
First approved in 1980
Class (Stereo):
CHEMICAL (ACHIRAL)
Targets:
Conditions:
Zomepirac Sodium (Zomax) is a pyrrole-acetic acid structurally related to tolmetin sodium. Zomepirac is a prostaglandin synthetase inhibitor and is not an opioid, an opioid antagonist, or a salicylate. Zomepirac was approved by the Food and Drug Administration for marketing in the United States as an analgesic. It was indicated for all forms of mild to moderately severe pain, and was being promoted as a "comprehensive, non-addicting analgesic." Later Zomepirac was found to be associated with fatal and near-fatal anaphylactoid reactions. The manufacturer voluntarily removed Zomax tablets from the Canadian, US, and UK markets in March 1983.
