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tablets for coadministration with statins no longer outweigh the risks, and the approval for this indication should be withdrawn.

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.

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.

Phosphate is a major intracellular anion in mammals. Hydrogen phopshate is a protonated form of phosphate. In serum, phosphate exists in two forms, dihydrogen phosphate (H2PO4) and its salt, mono-hydrogen phosphate (HPO4). At the physiologic pH of 7.40, the pK of H2PO4 is 6.8 and the ratio of HPO4 to H2PO4 is 4:1. Altered level of phosphate can be an indicator of various disorders, such as chronic renal failure, hypoparathyroidism, familial intermittent hyperphosphatemia, endocrine disorders, hyperthyroidism, acromegaly, juvenile hypogonadism, etc. These disorders may lead to either hyper- or hypophosphatemia, which can be caused by cellular shifts of phosphate. Patients with hypophosphatemia can be treated with dietary phosphate supplements (potassium phosphate, for example).

Pentaerythritol tetranitrate is an organic nitrate that has been used for the treatment of angina pectoris. Upon administration, the drug undergoes exstensive metabolism to NO which causes vasodilation and the relaxation of smooth muscle cells. The compound belongs to a familiy of explosive substances and may be used accordingly.

Potassium is needed to maintain good health. When potassium level falls below 3.5 mmol/L, Hypokalemia is diagnosed. In case of extremely low level of potassium (lower than 2.5 mmol/L) the following symptoms are appeared: malaise and fatigue. This low level of potassium can lead to severe muscle weakness and paralysis; respiratory failure; intermittent muscle spasms. It is known, foods that are good sources of potassium and low in sodium may reduce the risk of high blood pressure and stroke. Potassium supplementation is also recommended as an adjuvant antihypertensive agent for patients with essential hypertension.

SULFATE (as sodium sulfate, potassium sulfate, and magnesium sulfate) is a component of SUPREP Bowel Prep Kit. It is an osmotic laxative indicated for cleansing of the colon in preparation for colonoscopy in adults. Sulfate salts provide sulfate anions, which are poorly absorbed. The osmotic effect of unabsorbed sulfate anions and the associated cations causes water to be retained within the gastrointestinal tract. SUPREP Bowel Prep Kit, when ingested with a large volume of water, produces copious watery diarrhea.

SULFATE (as sodium sulfate, potassium sulfate, and magnesium sulfate) is a component of SUPREP Bowel Prep Kit. It is an osmotic laxative indicated for cleansing of the colon in preparation for colonoscopy in adults. Sulfate salts provide sulfate anions, which are poorly absorbed. The osmotic effect of unabsorbed sulfate anions and the associated cations causes water to be retained within the gastrointestinal tract. SUPREP Bowel Prep Kit, when ingested with a large volume of water, produces copious watery diarrhea.

Sodium lactate is primarily indicated as a source of bicarbonate for prevention or control of mild to moderate metabolic acidosis in patients with restricted oral intake whose oxidative processes are not seriously impaired. Sodium Lactate is most commonly associated with an E number of “E325” Sodium Lactate blends are commonly used in meat and poultry products to extend shelf life and increase food safety. They have a broad antimicrobial action and are effective at inhibiting most spoilage and pathogenic bacteria. In addition sodium lactate is used in cosmetics as a humectant, providing moisture.

There is no information about biological and pharmacological application of Iron(II) fluoride (also known as ferrous fluoride). It is known, that this substance is used to catalyze some organic reactions.