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Search results for angiotensin root_notes_note in Note (approximate match)
Status:
US Previously Marketed
Source:
Corrosive Mercuric Chloride U.S.P.
(1921)
Source URL:
First marketed in 1921
Source:
Corrosive Mercuric Chloride U.S.P.
Source URL:
Class (Stereo):
CHEMICAL (ACHIRAL)
Potassium Triiodomercurate(II) is a periodometallate salt. It contains a triiodomercurate(1-). It is an antiseptic (topical) and disinfectant. It is also an antiseborrheic agent.
Status:
US Previously Marketed
Source:
Lead Iodide N.F.
(1921)
Source URL:
First marketed in 1921
Class (Stereo):
CHEMICAL (ACHIRAL)
There is no information related to biological or pharmacological application of lead(II) bromide (a combustion product of the gasoline additives lead (IV) tetraethyl and 1,2-dibromoethane). It is only known, that this substance possesses mutagenicity.
Status:
US Previously Marketed
Source:
Oleic Acid U.S.P.
(1921)
Source URL:
First marketed in 1921
Class (Stereo):
CHEMICAL (ACHIRAL)
Targets:
Oleic acid is an unsaturated fatty acid that is the most widely distributed and abundant fatty acid in nature. It is used commercially in the preparation of oleates and lotions, and as a pharmaceutical solvent. Oleic acid occurs naturally in various animal and vegetable fats and oils. It is a component of the normal human diet as a part of animal fats and vegetable oils. Oleic acid may be responsible for the hypotensive (blood pressure reducing) effects of olive oil. Oleic acid has being shown to have a potential anticancer activity.
Status:
Possibly Marketed Outside US
First approved in 1982
Source:
NDA018467
Source URL:
Class (Stereo):
CHEMICAL (ACHIRAL)
Readily soluble in water, SnF2 is hydrolysed. At low concentration, it forms species such as SnOH+, Sn(OH)2 and Sn(OH)3−. At higher concentrations, predominantly polynuclear species are formed, including Sn2(OH)22+ and Sn3(OH)42+. Aqueous solutions readily oxidise to form insoluble precipitates of SnIV, which are ineffective as a dental prophylactic. Tin(II) fluoride, commonly referred to commercially (with tin(II) in Latin) as stannous fluoride, is a chemical compound with the formula SnF2. It is a colorless solid used as an ingredient in toothpastes that are typically more expensive than those that use sodium fluoride. Stannous fluoride has both bactericidal and bacteriostatic properties, which fight plaque and treat/prevent gingivitis. The stannous fluoride also deposits a protective mineral barrier over exposed dentinal tubules to help prevent sensitivity pain from triggers such as hot or cold liquids and foods. Stannous fluoride is used under the trade name "Fluoristan" in the original formulation of the toothpaste Crest, though it was later replaced with sodium monofluorophosphate, or "Fluoristat". It is the active ingredient in Crest Pro Health brand toothpaste. Crest Pro Health issues a warning on the tube that stannous fluoride may cause staining, which can be avoided by proper brushing, and that its particular formulation is resistant to staining. Any stannous fluoride staining that occurs due to improper brushing is not permanent. Stannous fluoride is also used in Oral-B Pro-Expert. Stannous fluoride is also readily available in over-the-counter rinses.
Status:
Possibly Marketed Outside US
Source:
NCT00004317: Phase 4 Interventional Recruiting Toxoplasmosis
(2000)
Source URL:
Class:
MIXTURE
Targets:
Spiramycin, a macrolide antibiotic, has been studied in the United States for the treatment of cryptosporidial diarrhea. Some reports suggest that spiramycin is useful in improving the symptoms of cryptosporidial diarrhea in some patients. It has been used in Europe and Canada for over 20 years to treat bacterial infections. Serious adverse effects from spiramycin are apparently rare, and no drug-associated deaths have been reported. Spiramycin inhibits translocation by binding to bacterial 50S ribosomal subunits with an apparent 1:1 stoichiometry. This antibiotic is a potent inhibitor of the binding to the ribosome of both donor and acceptor substrates. Spiramycin induces rapid breakdown of polyribosomes, an effect which has formerly been interpreted as occurring by normal ribosomal run-off followed by an antibiotic-induced block at or shortly after initiation of a new peptide. However, there is now convincing evidence that spiramycin, and probably all macrolides, act primarily by stimulating the dissociation of peptidyl-tRNA from ribosomes during translocation
Status:
US Approved Rx
(2017)
Source:
NDA209360
(2017)
Source URL:
First approved in 2017
Source:
NDA209360
Source URL:
Class:
PROTEIN
Angiotensin is a peptide hormone that causes vasoconstriction and a subsequent increase in blood pressure. It is part of the renin-angiotensin system, which is a major target for drugs that lower blood pressure. Angiotensin also stimulates the release of aldosterone, another hormone, from the adrenal cortex. Aldosterone promotes sodium retention in the distal nephron, in the kidney, which also drives blood pressure up. Angiotensin is an oligopeptide and is a hormone and a powerful dipsogen. Angiotensin I is derived from the precursor molecule angiotensinogen, a serum globulin produced in the liver. Angiotensin I is converted to angiotensin II (AII) through removal of two C-terminal residues by the enzyme angiotensin-converting enzyme (ACE), primarily through ACE within the lung (but also present in endothelial cells and kidney epithelial cells). ACE found in other tissues of the body has no physiological role (ACE has a high density in the lung, but activation here promotes no vasoconstriction, angiotensin II is below physiological levels of action). Angiotensin II acts as an endocrine, autocrine/paracrine, and intracrine hormone. Angiotensin II has prothrombotic potential through adhesion and aggregation of platelets and stimulation of PAI-1 and PAI-2. When cardiac cell growth is stimulated, a local (autocrine-paracrine) renin-angiotensin system is activated in the cardiac myocyte, which stimulates cardiac cell growth through protein kinase C. The same system can be activated in smooth muscle cells in conditions of hypertension, atherosclerosis, or endothelial damage. Angiotensin II is the most important Gq stimulator of the heart during hypertrophy, compared to endothelin-1 and α1 adrenoreceptors. Angiotensin II increases thirst sensation (dipsogen) through the subfornical organ of the brain, decreases the response of the baroreceptor reflex, and increases the desire for salt. It increases secretion of ADH in the posterior pituitary and secretion of ACTH in the anterior pituitary. It also potentiates the release of norepinephrine by direct action on postganglionic sympathetic fibers. Angiotensin II acts on the adrenal cortex, causing it to release aldosterone, a hormone that causes the kidneys to retain sodium and lose potassium. Elevated plasma angiotensin II levels are responsible for the elevated aldosterone levels present during the luteal phase of the menstrual cycle. Angiotensin II has a direct effect on the proximal tubules to increase Na+ reabsorption. It has a complex and variable effect on glomerular filtration and renal blood flow depending on the setting. Increases in systemic blood pressure will maintain renal perfusion pressure; however, constriction of the afferent and efferent glomerular arterioles will tend to restrict renal blood flow. The effect on the efferent arteriolar resistance is, however, markedly greater, in part due to its smaller basal diameter; this tends to increase glomerular capillary hydrostatic pressure and maintain glomerular filtration rate. A number of other mechanisms can affect renal blood flow and GFR. High concentrations of Angiotensin II can constrict the glomerular mesangium, reducing the area for glomerular filtration. Angiotensin II is a sensitizer to tubuloglomerular feedback, preventing an excessive rise in GFR. Angiotensin II causes the local release of prostaglandins, which, in turn, antagonize renal vasoconstriction. The net effect of these competing mechanisms on glomerular filtration will vary with the physiological and pharmacological environment. Angiotensin was independently isolated in Indianapolis and Argentina in the late 1930s (as 'angiotonin' and 'hypertensin', respectively) and subsequently characterised and synthesized by groups at the Cleveland Clinic and Ciba laboratories in Basel, Switzerland.