NIACIN- niacin tablet
Redmont Pharmaceuticals, LLC


Niacin or nicotinic acid, a water-soluble B‑complex vitamin and antihyperlipidemic agent, is 3‑pyridinecarboxylic acid. It is a white, crystalline powder, sparingly soluble in water. It has the following structural formula:

MW=123.11Chemical StructureC6 H5 NO2

Each Niacin Tablet, for oral administration, contains 500 mg of nicotinic acid. In addition, each tablet contains the following inactive ingredients: croscarmellose sodium, hydrogenated vegetable oil, magnesium stearate and microcrystalline cellulose.


The role of low-density lipoprotein (LDL) cholesterol in atherogenesis is supported by pathological observations, clinical studies, and many animal experiments. Observational epidemiological studies have clearly established that high total or LDL cholesterol and low high-density lipoprotein (HDL) cholesterol are risk factors for coronary heart disease. The Coronary Drug Project1 , completed in 1975, was designed to assess the safety and efficacy of nicotinic acid and other lipid-altering drugs in men 30 to 64 years old with a history of myocardial infarction (MI). Over an observation period of five years, nicotinic acid showed a statistically significant benefit in decreasing nonfatal, recurrent myocardial infarctions. The incidence of definite, nonfatal MI was 8.9% for the 1,119 patients randomized to nicotinic acid versus 12.2% for the 2,789 patients who received placebo (p< 0.004). Though total mortality was similar in the two groups at five years (24.4% with nicotinic acid versus 25.4% with placebo; p=N.S.), in a fifteen year cumulative follow-up there were 11% (69) fewer deaths in the nicotinic acid group compared to the placebo cohort (52.0% versus 58.2%; p=0.0004)2.

The Cholesterol-Lowering Atherosclerosis Study (CLAS) was a randomized, placebo-controlled, angiographic trial testing combined colestipol and nicotinic acid therapy in 162 non-smoking males with previous coronary bypass surgery3. The primary, per subject cardiac endpoint was global coronary artery change score. After two years, 61% of patients in the placebo cohort showed disease progression by global change score (N=82), compared with only 38.8% of drug-treated subjects (N=80), when both native arteries and grafts were considered (p<0.005). In a follow-up to this trial in a subgroup of 103 patients treated for four years, again, significantly fewer patients in the drug-treated group demonstrated progression than in the placebo cohort (48% versus 85%, respectively; p< 0.0001)4.

The Familial Atherosclerosis Treatment Study (FATS) in 146 men ages 62 and younger with apolipoprotein B levels ≥125 mg/dL, established coronary artery disease, and family histories of vascular disease, assessed change in severity of disease in the proximal coronary arteries by quantitative arteriography5. Patients were given dietary counseling and randomized to treatment with either conventional therapy with double placebo (or placebo plus colestipol if the LDL cholesterol was elevated); lovastatin plus colestipol; or nicotinic acid plus colestipol. In the conventional therapy group, 46% of patients had disease progression (and no regression) in at least one of nine proximal coronary segments. In contrast, progression (as the only change) was seen in only 25% in the nicotinic acid plus colestipol group. Though not an original endpoint of the trial, clinical events (death, myocardial infarction, or revascularization for worsening angina) occurred in 10 of 52 patients who received conventional therapy, compared with 2 of 48 who received nicotinic acid plus colestipol.

Nicotinic acid (but not nicotinamide) in gram doses produces an average 10% to 20% reduction in total and LDL cholesterol, a 30% to 70% reduction in triglycerides, and an average 20% to 35% increase in HDL cholesterol. The magnitude of individual lipid and lipoprotein responses may be influenced by the severity and type of underlying lipid abnormality. The increase in total HDL is associated with a shift in the distribution of HDL sub-fractions (as defined by ultra-centrifugation) with an increase in the HDL2 :HDL3 ratio and an increase in apolipoprotein A‑I content. The mechanism by which nicotinic acid exerts these effects is not entirely understood, but may involve several actions, including a decrease in esterification of hepatic triglycerides. Nicotinic acid treatment also decreases the serum levels of apolipoprotein B‑100 (apo B), the major protein component of the very low-density lipoprotein (VLDL) and LDL fractions, and of lipoprotein a [Lp(a)], a variant form of LDL independently associated with coronary risk. The effect of nicotinic acid-induced changes in lipids/lipoproteins on cardiovascular morbidity or mortality in individuals without pre-existing coronary disease has not been established.


Following an oral dose, the pharmacokinetic profile of nicotinic acid is characterized by rapid absorption from the gastrointestinal tract and a short plasma elimination half-life. At a 1 gram dose, peak plasma concentrations of 15 to 30 µg/mL are reached within 30 to 60 minutes. Approximately 88% of an oral pharmacologic dose is eliminated by the kidneys as unchanged drug and nicotinuric acid, its primary metabolite. The plasma elimination half-life of nicotinic acid ranges from 20 to 45 minutes.


I. Therapy with lipid-altering agents should be only one component of multiple risk factor intervention in those individuals at significantly increased risk for atherosclerotic vascular disease due to hypercholesterolemia. Nicotinic acid, alone or in combination with a bile-acid binding resin, is indicated as an adjunct to diet for the reduction of elevated total and LDL cholesterol levels in patients with primary hypercholesterolemia (Types IIa and IIb) , when the response to a diet restricted in saturated fat and cholesterol and other nonpharmacologic measures alone has been inadequate (see also the NCEP treatment guidelines6). Prior to initiating therapy with nicotinic acid, secondary causes for hypercholesterolemia (e.g., poorly controlled diabetes mellitus, hypothyroidism, nephrotic syndrome, dysproteinemias, obstructive liver disease, other drug therapy, alcoholism) should be excluded, and a lipid profile performed to measure total cholesterol, HDL cholesterol, and triglycerides.

II. Nicotinic acid is also indicated as adjunctive therapy for the treatment of adult patients with very high serum triglyceride levels (Types IV and V hyperlipidemia) who present a risk of pancreatitis and who do not respond adequately to a determined dietary effort to control them. Such patients typically have serum triglyceride levels over 2,000 mg/dL and have elevations of VLDL cholesterol as well as fasting chylomicrons (Type V hyperlipidemia). Subjects who consistently have total serum or plasma triglycerides below 1,000 mg/dL are unlikely to develop pancreatitis. Therapy with nicotinic acid may be considered for those subjects with triglyceride elevations between 1,000 and 2,000 mg/dL who have a history of pancreatitis or of recurrent abdominal pain typical of pancreatitis. Some Type IV patients with triglycerides under 1,000 mg/dL may, through dietary or alcoholic indiscretion, convert to a Type V pattern with massive triglyceride elevations accompanying fasting chylomicronemia, but the influence of nicotinic acid therapy on the risk of pancreatitis in such situations has not been adequately studied. Drug therapy is not indicated for patients with Type I hyperlipoproteinemia, who have elevations of chylomicrons and plasma triglycerides, but who have normal levels of VLDL. Inspection of plasma refrigerated for 14 hours is helpful in distinguishing Types I, IV, and V hyperlipoproteinemia7.

Classification of Hyperlipoproteinemias
Lipoproteins Lipid Elevations
Type Elevated Major Minor
C = cholesterol, TG = triglycerides
LDL = low-density lipoprotein
VLDL = very low-density lipoprotein
IDL = intermediate-density lipoprotein
I (rare) Chylomicrons TG ↑→ C
IIa LDL C …..
III (rare) IDL C/TG …..
V (rare) Chylomicrons, VLDL TG ↑→ C
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