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Search results for "ascorbic acid" in Standardized Name (approximate match)
Status:
US Previously Marketed
Source:
Pre-Creatine glycocyamine by Mercury Pharmaceuticals
(1958)
Source URL:
First approved in 1958
Source:
Pre-Creatine glycocyamine by Mercury Pharmaceuticals
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Status:
US Previously Marketed
Source:
SANDRIL by LILLY
(1982)
Source URL:
First approved in 1954
Source:
SERPASIL by NOVARTIS
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Conditions:
Reserpine is an alkaloid, isolated from the Rauwolfia serpentina plant and developed by Ciba pharma. Reserpine was approved by FDA for the treatment of hypertension and psychotic disorders. The drug exerts its effect by blocking two vesicular monoamine transporters, VMAT1 and VMAT2. The blockade results in vesicles that lose their ability to store neurotransmitter molecules. Neurotransmitters, thus retained in cytosol, are then neutralized by MAO.
Status:
US Previously Marketed
Source:
PRELU-VITE IRON by GEIGY
(1961)
Source URL:
First marketed in 1921
Class (Stereo):
CHEMICAL (ABSOLUTE)
Direct reduced iron is an alternative iron source produced by heating an iron ore. In nature, most of the iron has an oxidized form.
Status:
US Previously Marketed
Source:
TETRACYN by PFIZER
(1954)
Source URL:
First marketed in 1905
Class (Stereo):
CHEMICAL (ABSOLUTE)
Targets:
Conditions:
Procaine is an anesthetic agent indicated for production of local or regional anesthesia, particularly for oral surgery. Procaine (like cocaine) has the advantage of constricting blood vessels which reduces bleeding, unlike other local anesthetics like lidocaine. Procaine is an ester anesthetic. It is metabolized in the plasma by the enzyme pseudocholinesterase through hydrolysis into para-aminobenzoic acid (PABA), which is then excreted by the kidneys into the urine. Procaine acts mainly by inhibiting sodium influx through voltage gated sodium channels in the neuronal cell membrane of peripheral nerves. When the influx of sodium is interrupted, an action potential cannot arise and signal conduction is thus inhibited. The receptor site is thought to be located at the cytoplasmic (inner) portion of the sodium channel. Procaine has also been shown to bind or antagonize the function of N-methyl-D-aspartate (NMDA) receptors as well as nicotinic acetylcholine receptors and the serotonin receptor-ion channel complex.
Status:
US Previously Marketed
Source:
ALLONAL AMINOPHENAZONE by ROCHE
(1921)
Source URL:
First marketed in 1897
Class (Stereo):
CHEMICAL (ABSOLUTE)
Targets:
Conditions:
Aminophenazone is a phenyl-pyrazolone derivative with potent analgesic and antipyretic properties. Aminophenazone has been used as salt or complexes, including topically as the salicylate. It was recommended for the treatment of a fever, neuralgia, myositis, acute rheumatism, arthritis, chorea. In 1999 the FDA suspended aminophenazone. The drug caused agranulocytosis. Some of the cases of agranulocytosis were fatal. Another reason for suspending this drug from the market was its ability to react with nitrite-containing food, thus forming carcinogenic nitrosamines. A breath test with 13C-labeled aminopyrine has been used as a non-invasive measure of cytochrome P-450 metabolic activity in liver function tests.
Status:
Possibly Marketed Outside US
Source:
Pro Hers Vanilla by CROWN GENERAL AGENCY INC
Source URL:
First approved in 1996
Source:
Strovite Forte Caplet by Everett Laboratories, Inc.
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Molybdenum (Mo) is an essential trace element and is a component of vitamin and mineral supplements. Molybdenum has essential biological roles in organisms and microorganisms. Molybdenum is the only trace metal of the second
row of the periodic table that exhibits biological activity
when it is ligated to a cofactor. It acts as a critical cofactor in several molybdenum-dependent enzymes that are involved in important cellular reactions and pathways, including xanthine oxidoreductase. In nature two principal
concepts of Mo cofactors have evolved, one is the iron Mo
cofactor in bacterial nitrogenase and the other is represented by a large family of enzymes with more than
100 representatives relying on the pterin-based Mo cofactor (Moco). Moco-containing enzymes catalyze key
redox reactions in the global carbon, sulfur and nitrogen
cycles. Four molybdenum-dependent enzymes are known in humans, each harboring a pterin-based molybdenum cofactor (Moco) in the active site. In these enzymes, molybdenum catalyzes oxygen transfer reactions from or to substrates using water as oxygen donor or acceptor. Molybdenum shuttles between two oxidation states, Mo(IV) and Mo(VI). Following substrate reduction or oxidation, electrons are subsequently shuttled by either inter- or intra-molecular electron transfer chains involving prosthetic groups such as heme or iron-sulfur clusters. In all organisms studied so far, Moco is synthesized by a highly conserved multi-step biosynthetic pathway. A deficiency in the biosynthesis of Moco results in a pleitropic loss of all four human Mo-enzyme activities and in most cases in early childhood death. For the general population, the diet is the most important source of molybdenum and concentrations in water and air usually are negligible. The average daily dietary intake is about 0.1-0.5 mg m.o. Molybdenum is marketed both as a tablet and as a liquid supplement containing the mineral in dissolved form. Despite widespread claims, there is no evidence that one form of molybdenum is absorbed to a markedly superior extent than any other. Current marketing of molybdenum products for the treatment of medical conditions is not founded on any meaningful scientific evidence. People with serious kidney disease should avoid taking molybdenum (or any other supplement) except on the advice of a physician. People with serious kidney disease should also avoid taking molybdenum (or any other supplement) except on the advice of a physician.