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Restrict the search for
niacin
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There is one exact (name or code) match for niacin
Status:
US Approved Rx
(2022)
Source:
ANDA204934
(2022)
Source URL:
First marketed in 1937
Class (Stereo):
CHEMICAL (ACHIRAL)
Targets:
Niacin (also known as vitamin B3 and nicotinic acid) is bio converted to nicotinamide which is further converted to nicotinamide adenine dinucleotide (NAD+) and the hydride equivalent (NADH) which are coenzymes necessary for tissue metabolism, lipid metabolism, and glycogenolysis. Niacin (but not nicotinamide) in gram doses reduces LDL-C, Apo B, Lp(a), TG, and TC, and increases HDL-C. The increase in HDL-C is associated with an increase in apolipoprotein A-I (Apo A-I) and a shift in the distribution of HDL subfractions. These shifts include an increase in the HDL2:HDL3 ratio, and an elevation in lipoprotein A-I (Lp A-I, an HDL-C particle containing only Apo A-I). The mechanism by which niacin alters lipid profiles is not completely understood and may involve several actions, including partial inhibition of release of free fatty acids from adipose tissue, and increased lipoprotein lipase activity (which may increase the rate of chylomicron triglyceride removal from plasma). Niacin decreases the rate of hepatic synthesis of VLDL-C and LDL-C, and does not appear to affect fecal excretion of fats, sterols, or bile acids. As an adjunct to diet, the efficacy of niacin and lovastatin in improving lipid profiles (either individually, or in combination with each other, or niacin in combination with other statins) for the treatment of dyslipidemia has been well documented. The effect of combined therapy with niacin and lovastatin on cardiovascular morbidity and mortality has not been determined. In addition, preliminary reports suggest that niacin causes favorable LDL particle size transformations, although the clinical relevance of this effect is not yet clear. April 15, 2016: Based on several large cardiovascular outcome trials including AIM-HIGH, ACCORD, and HPS2-THRIVE, the FDA decided that "scientific evidence no longer supports the conclusion that a drug-induced reduction in triglyceride levels and/or increase in HDL-cholesterol levels in statin-treated patients results in a reduction in the risk of cardiovascular events" Consistent with this conclusion, the FDA has determined that the benefits of niacin ER tablets for coadministration with statins no longer outweigh the risks, and the approval for this indication should be withdrawn.
Status:
US Approved Rx
(2022)
Source:
ANDA204934
(2022)
Source URL:
First marketed in 1937
Class (Stereo):
CHEMICAL (ACHIRAL)
Targets:
Niacin (also known as vitamin B3 and nicotinic acid) is bio converted to nicotinamide which is further converted to nicotinamide adenine dinucleotide (NAD+) and the hydride equivalent (NADH) which are coenzymes necessary for tissue metabolism, lipid metabolism, and glycogenolysis. Niacin (but not nicotinamide) in gram doses reduces LDL-C, Apo B, Lp(a), TG, and TC, and increases HDL-C. The increase in HDL-C is associated with an increase in apolipoprotein A-I (Apo A-I) and a shift in the distribution of HDL subfractions. These shifts include an increase in the HDL2:HDL3 ratio, and an elevation in lipoprotein A-I (Lp A-I, an HDL-C particle containing only Apo A-I). The mechanism by which niacin alters lipid profiles is not completely understood and may involve several actions, including partial inhibition of release of free fatty acids from adipose tissue, and increased lipoprotein lipase activity (which may increase the rate of chylomicron triglyceride removal from plasma). Niacin decreases the rate of hepatic synthesis of VLDL-C and LDL-C, and does not appear to affect fecal excretion of fats, sterols, or bile acids. As an adjunct to diet, the efficacy of niacin and lovastatin in improving lipid profiles (either individually, or in combination with each other, or niacin in combination with other statins) for the treatment of dyslipidemia has been well documented. The effect of combined therapy with niacin and lovastatin on cardiovascular morbidity and mortality has not been determined. In addition, preliminary reports suggest that niacin causes favorable LDL particle size transformations, although the clinical relevance of this effect is not yet clear. April 15, 2016: Based on several large cardiovascular outcome trials including AIM-HIGH, ACCORD, and HPS2-THRIVE, the FDA decided that "scientific evidence no longer supports the conclusion that a drug-induced reduction in triglyceride levels and/or increase in HDL-cholesterol levels in statin-treated patients results in a reduction in the risk of cardiovascular events" Consistent with this conclusion, the FDA has determined that the benefits of niacin ER tablets for coadministration with statins no longer outweigh the risks, and the approval for this indication should be withdrawn.
Status:
US Approved Rx
(2001)
Source:
NDA021265
(2001)
Source URL:
First approved in 1947
Source:
BEROCCA PN by ROCHE
Source URL:
Class (Stereo):
CHEMICAL (ACHIRAL)
Targets:
Niacinamide, known as nicotinamide, is an important compound functioning as a component of the coenzyme NAD. Its primary significance is in the prevention and/or cure of blacktongue and pellagra. Pellagra is a nutritional disease that occurs due to insufficient dietary amounts of vitamin B3 or the chemical it is made from (tryptophan). Symptoms of pellagra include skin disease, diarrhea, dementia, and depression. In addition, was experiments, revealed, that niacinamide hydroiodide might have role in ophthalmology and parenteral use of niacinamide hydroiodide can treat arteriosclerotic syndromes.
Status:
US Approved OTC
Source:
21 CFR 350.10(l) antiperspirant aluminum zirconium octachlorohydrex gly
Source URL:
First marketed in 1903
Source:
EverDry by EverDry
Source URL:
Class (Stereo):
CHEMICAL (ACHIRAL)
Burow invented an astringent antiseptic solution of aluminium acetate in water to relieve the itching and inflammation of minor skin irritations. At present the oflicial U. S. P. procedure to made Burow's solution involves the reaction of aluminum sulfate, calcium carbonate and acetic acid to form aluminum sub-acetate, also termed basic aluminum acetate.
The solution is available as an over-the-counter drug for topical administration, with brand names including Domeboro. Burow's solution has been shown to be effective against chronic suppurative otitis media and otitis externa. It is active against bacteria resulting in damage to the cell wall.
Status:
Investigational
Source:
NCT00847197: Phase 2 Interventional Completed Dyslipidemia
(2008)
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Conditions:
MK-1903 is a potent and selective hydroxycarboxylic acid receptor 2 (HCA2, GPR109A) full agonist. Exhibits no binding at the GRP109B receptor. This drug had been in phase II clinical trial for the treatment of atherosclerosis and Dyslipidemia. But then, according to Merck, elevation of HDL cholesterol relative to placebo did not meet the trial's pre-specified primary objective for efficacy; no safety signals were implicated as drivers of the decision to discontinue development.
Status:
Investigational
Source:
NCT00758303: Phase 2/Phase 3 Interventional Completed Hyperlipidemia
(2007)
Source URL:
Class (Stereo):
CHEMICAL (ACHIRAL)
Targets:
Conditions:
Trigonellamide (1-Methylnicotinamide) is a metabolite of nicotinamide and is produced primarily in the liver by nicotinamide N-methyltransferase. Trigonellamide may be an endogenous activator of prostacyclin (PGI2) production and thus may regulate thrombotic as well as inflammatory processes in the cardiovascular system. The mechanisms of action of Trigonellamide involve the activation of PGI2 release driven by cyclooxygenase 2 (COX-2). PGI2 releasing capacity of 1- Trigonellamide was shown to afford not only anti-thrombotic but also fibrinolytic, anti-inflammatory and gastroprotective effects. Interestingly, Trigonellamide did not directly either affect the activity of leucocytes or release PGI2 in the perfused rat hindquarters model. Still, Trigonellamide, due to its PGI2 releasing capacity, might serve as a hepatoprotective agent that protects against Concanavalin-A induced liver injury through the downregulation of interleukin-4 (IL-4) and tumor necrosis factor-α signalization (TNF-α). In addition to its anti-platelet, anti-thrombotic and anti-inflammatory activities, 1-MNA has also been shown to restore endothelial function in diabetic hyperglycemic rats, as well as to improve endothelial function in humans. PGI2 displays anti-metastatic activity, and the PGI2 releasing activity of Trigonellamide, the potential application of exogenous Trigonellamide to prevent metastatic cancer.
Class (Stereo):
CHEMICAL (ABSOLUTE)
Glunicate (LG 13979) is a long-acting nicotinic acid derivative that can lower plasma triglyceride levels, while leaving other lipoprotein parameters unaffected. It exerts a dose‐dependent reduction of plasma triglycerides and cholesterol. In rabbits, glunicate provided dose-dependent protection of the arterial wall from atheromatous lesions and from cholesterol and collagen accumulation. It has been shown that glunicate has prolonged activity on plasma free fatty acids and triglycerides, with long lasting and intense activity on plasma cholesterol.
Status:
Investigational
Source:
INN:oxiniacic acid [INN]
Source URL:
Class (Stereo):
CHEMICAL (ACHIRAL)
Conditions:
Oxiniacic Acid is a nicotinic acid derivative, that shows potent hypolipidemic activity.
Status:
Other
Class (Stereo):
CHEMICAL (ACHIRAL)
Conditions:
Zinc Nicotinate is a mineral powder that is essential for the immune system, enzymes, hormones, the reproductive system, and the skeletal system. It is a functional food nutritional ingredient.
