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Search results for aminolevulinic root_references_citation in Reference Text / Citation (approximate match)
Status:
US Previously Marketed
Source:
21 CFR 310.545(a)(20) weight control leucine
Source URL:
First approved in 1971
Source:
NDA016822
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Leucine is an α-amino acid used in the biosynthesis of proteins. Leucine is an essential hydrophobic amino acid. It is used in the Leucine may be used some people as a supplement to build muscle. Leucine is also found in fish, meat, and poultry. In the pharmaceutical industry, L-leucine is used for parenteral and enteral nutrition and feeding, and is also used as a flavoring product and tablet lubricant in manufacturing. Leucine is an mTOR activator. It is a dietary amino acid with the capacity to directly stimulate muscle protein synthesis. As a dietary supplement, leucine has been found to slow the degradation of muscle tissue by increasing the synthesis of muscle proteins in aged rats. Long-term leucine supplementation does not increase muscle mass or strength in healthy elderly men. Leucine potently activates the mammalian target of rapamycin kinase that regulates cell growth. Infusion of leucine into the rat brain has been shown to decrease food intake and body weight via activation of the mTOR pathway.
Status:
US Previously Marketed
Source:
ATROMID-S by WYETH AYERST
(1967)
Source URL:
First approved in 1967
Source:
ATROMID-S by WYETH AYERST
Source URL:
Class (Stereo):
CHEMICAL (ACHIRAL)
Targets:
Conditions:
Clofibrate is a fibric acid derivative used to lower cholesterol and triglyceride (fat-like substances) levels in the blood. This may help prevent medical problems caused by such substances clogging the blood vessels. However, this treatment was discontinued in 2002 due to adverse effects. Clofibrate is an agonist of the PPAR-α receptor in muscle, liver, and other tissues. This agonism ultimately leads to modification in gene expression resulting in increased beta-oxidation, decreased triglyceride secretion, increased HDL, and increased lipoprotein lipase activity. Clofibrate increased the activity of extrahepatic lipoprotein lipase (LL), thereby increasing lipoprotein triglyceride lipolysis, inhibited the synthesis, and increases the clearance of apolipoprotein B, a carrier molecule for VLDL. In addition, clofibrate was investigated as a novel therapy agent in multiple myeloma and it shown the promising results.
Status:
US Previously Marketed
Source:
ATROMID-S by WYETH AYERST
(1967)
Source URL:
First approved in 1967
Source:
ATROMID-S by WYETH AYERST
Source URL:
Class (Stereo):
CHEMICAL (ACHIRAL)
Targets:
Conditions:
Clofibrate is a fibric acid derivative used to lower cholesterol and triglyceride (fat-like substances) levels in the blood. This may help prevent medical problems caused by such substances clogging the blood vessels. However, this treatment was discontinued in 2002 due to adverse effects. Clofibrate is an agonist of the PPAR-α receptor in muscle, liver, and other tissues. This agonism ultimately leads to modification in gene expression resulting in increased beta-oxidation, decreased triglyceride secretion, increased HDL, and increased lipoprotein lipase activity. Clofibrate increased the activity of extrahepatic lipoprotein lipase (LL), thereby increasing lipoprotein triglyceride lipolysis, inhibited the synthesis, and increases the clearance of apolipoprotein B, a carrier molecule for VLDL. In addition, clofibrate was investigated as a novel therapy agent in multiple myeloma and it shown the promising results.
Status:
US Previously Marketed
Source:
ATROMID-S by WYETH AYERST
(1967)
Source URL:
First approved in 1967
Source:
ATROMID-S by WYETH AYERST
Source URL:
Class (Stereo):
CHEMICAL (ACHIRAL)
Targets:
Conditions:
Clofibrate is a fibric acid derivative used to lower cholesterol and triglyceride (fat-like substances) levels in the blood. This may help prevent medical problems caused by such substances clogging the blood vessels. However, this treatment was discontinued in 2002 due to adverse effects. Clofibrate is an agonist of the PPAR-α receptor in muscle, liver, and other tissues. This agonism ultimately leads to modification in gene expression resulting in increased beta-oxidation, decreased triglyceride secretion, increased HDL, and increased lipoprotein lipase activity. Clofibrate increased the activity of extrahepatic lipoprotein lipase (LL), thereby increasing lipoprotein triglyceride lipolysis, inhibited the synthesis, and increases the clearance of apolipoprotein B, a carrier molecule for VLDL. In addition, clofibrate was investigated as a novel therapy agent in multiple myeloma and it shown the promising results.
Status:
US Previously Marketed
Source:
DIDRONEL by MGI PHARMA INC
(1987)
Source URL:
First approved in 1965
Source:
M006
Source URL:
Class (Stereo):
CHEMICAL (ACHIRAL)
Targets:
Etidronate is a salt of etidronic acid (brand name Didronel, also known as EHDP) a diphosphonate, which is indicated for the treatment of symptomatic Paget’s disease of bone and in the prevention and treatment of heterotopic ossification following total hip replacement or due to spinal cord injury. Didronel is not approved for the treatment of osteoporosis. This drugs acts primarily on bone. It can inhibit the formation, growth, and dissolution of hydroxyapatite crystals and their amorphous precursors by chemisorption to calcium phosphate surfaces. Inhibition of crystal resorption occurs at lower doses than are required to inhibit crystal growth. Both effects increase as the dose increases. Preclinical studies indicate etidronate disodium does not cross the blood-brain barrier. Didronel is not metabolized. The amount of drug absorbed after an oral dose is approximately 3 percent. Bisphosphonates, when attached to bone tissue, are absorbed by osteoclasts, the bone cells that breaks down bone tissue. Although the mechanism of action of non-nitrogenous bisphosphonates has not been fully elucidated, available data suggest that they bind strongly to hydroxyapatite crystals in the bone matrix, preferentially at the sites of increased bone turnover and inhibit the formation and dissolution of the crystals. Other actions may include direct inhibition of mature osteoclast function, promotion of osteoclast apoptosis, and interference with osteoblast-mediated osteoclast activation. Etidronic acid may promote osteoclast apoptosis by competing with adenosine triphosphate (ATP) in the cellular energy metabolism. The osteoclast initiates apoptosis and dies, leading to an overall decrease in the breakdown of bone.
Status:
US Previously Marketed
Source:
DIDRONEL by MGI PHARMA INC
(1987)
Source URL:
First approved in 1965
Source:
M006
Source URL:
Class (Stereo):
CHEMICAL (ACHIRAL)
Targets:
Etidronate is a salt of etidronic acid (brand name Didronel, also known as EHDP) a diphosphonate, which is indicated for the treatment of symptomatic Paget’s disease of bone and in the prevention and treatment of heterotopic ossification following total hip replacement or due to spinal cord injury. Didronel is not approved for the treatment of osteoporosis. This drugs acts primarily on bone. It can inhibit the formation, growth, and dissolution of hydroxyapatite crystals and their amorphous precursors by chemisorption to calcium phosphate surfaces. Inhibition of crystal resorption occurs at lower doses than are required to inhibit crystal growth. Both effects increase as the dose increases. Preclinical studies indicate etidronate disodium does not cross the blood-brain barrier. Didronel is not metabolized. The amount of drug absorbed after an oral dose is approximately 3 percent. Bisphosphonates, when attached to bone tissue, are absorbed by osteoclasts, the bone cells that breaks down bone tissue. Although the mechanism of action of non-nitrogenous bisphosphonates has not been fully elucidated, available data suggest that they bind strongly to hydroxyapatite crystals in the bone matrix, preferentially at the sites of increased bone turnover and inhibit the formation and dissolution of the crystals. Other actions may include direct inhibition of mature osteoclast function, promotion of osteoclast apoptosis, and interference with osteoblast-mediated osteoclast activation. Etidronic acid may promote osteoclast apoptosis by competing with adenosine triphosphate (ATP) in the cellular energy metabolism. The osteoclast initiates apoptosis and dies, leading to an overall decrease in the breakdown of bone.
Status:
First approved in 1962
Class (Stereo):
CHEMICAL (ACHIRAL)
Conditions:
Phytate Sodium is a complex sodium salt of the corn-derived plant component Phytic Acid , that used as a chelating agent in all types of cosmetic products, including soaps, shampoos, balms and leave-on products for the face or body. Phytate Sodium is a biodegradable product and appears in the form of a dark-coloured liquid, is soluble in water and has a characteristic odour. It can be used in all types of cosmetic products, including soaps, shampoos, balms and leave-on products for the face or body. In vivo and in vitro experiments have demonstrated striking anticancer (preventive as well as therapeutic) effects of phytic acid. Research shows anti-carcinogenic effects, albeit to a lesser extent and it acts in inhibiting cancer. In addition to reduction in cell proliferation, phytic acid increases differentiation of malignant cells often resulting in reversion to the normal phenotype. Phytates participation in important intracellular biochemical pathways, normal physiological presence in human cells, tissues, plasma, urine, etc., the levels of which fluctuate with intake, epidemiological correlates of phytate deficiency with disease and reversal of those conditions by adequate intake, and safety – all strongly suggest for phytates inclusion as an essential nutrient, perhaps a vitamin. Phytic acid, mostly as Phytate Sodium or other phytates, is found within the hulls of nuts, seeds, and grains. No detectable phytate (less than 0.02 % of wet weight) was observed in vegetables such as scallion and cabbage leaves or in fruits such as apples, oranges, bananas, or pears. In-home food preparation techniques can break down the phytic acid in all of these foods. Simply cooking the food will reduce the phytic acid to some degree. More effective methods are soaking in an acid medium, sprouting and lactic acid fermentation such as in sourdough and pickling.
Status:
US Previously Marketed
Source:
KANAMYCIN SULFATE by FRESENIUS KABI USA
(2002)
Source URL:
First approved in 1958
Class (Stereo):
CHEMICAL (ABSOLUTE)
Targets:
Conditions:
Kanamycin A is aminoglycoside anti-bacterial agent. Active against many strains of Gram-negative bacteria and Gram-positive Staphylococcus aureus and epidermis. Some strains of Mycobacterium bacterium are sensitive. Most active in alkaline solution. It binds to bacterial ribosomes and reduces mRNA translation hence reduces protein biosynthesis. However, it also exhibits some toxic effects towards mammalian cells.
Status:
US Previously Marketed
Source:
TELEPAQUE by GE HEALTHCARE
(1951)
Source URL:
First approved in 1951
Source:
TELEPAQUE by GE HEALTHCARE
Source URL:
Class (Stereo):
CHEMICAL (RACEMIC)
Conditions:
Iopanoic acid is a representative iodinated ionic monomeric contrast medium.
Status:
First approved in 1949
Class (Stereo):
CHEMICAL (ABSOLUTE)
Conditions:
Adenosine monophosphate (AMP) is a nucleotide, consisting of a phosphate group, the sugar ribose, and the nucleobase adenine. AMP is an activator of several enzymes in the tissues. In the glycolytic pathway, the enzyme phosphofructokinase is inhibited by ATP but the inhibition is reversed by AMP, the deciding factor for the reaction being the ratio between ATP and AMP. In medicine, AMP is used mainly as an alternative to adenosine for treatment of ischemia and as a tool compound to measure hyperresponsiveness of airways.