DRUGS & SUPPLEMENTS
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:
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 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 fifteenyear 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 10-20% reduction in total and LDL cholesterol, a 30-70% reduction in triglycerides, and an average 20-35% 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 subfractions (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.
INDICATIONS AND USAGE
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 †, 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 2000 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 1000 mg/dL are unlikely to develop pancreatitis. Therapy with nicotinic acid may be considered for those subjects with triglyceride elevations between 1000 and 2000 mg/dL who have a history of pancreatitis or of recurrent abdominal pain typical of pancreatitis. Some Type IV patients with triglycerides under 1000 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.
Nicotinic acid is contraindicated in patients with a known hypersensitivity to any component of this medication; significant or unexplained hepatic dysfunction; active peptic ulcer disease; or arterial bleeding.
SPL UNCLASSIFIED SECTION
Cases of severe hepatic toxicity, including fulminant hepatic necrosis have occurred in patients who have substituted sustained-release nicotinic acid products for immediate-release (crystalline) nicotinic acid at equivalent doses.
Liver function tests should be performed on all patients during therapy with nicotinic acid. Serum transaminase levels, including ALT (SGPT), should be monitored before treatment begins, every six weeks to twelve weeks for the first year, and periodically thereafter (e.g., at approximately 6 month intervals). Special attention should be paid to patients who develop elevated serum transaminase levels, and in these patients, measurements should be repeated promptly and then performed more frequently. If the transaminase levels show evidence of progression, particularly if they rise to three times the upper limit of normal and are persistent, the drug should be discontinued. Liver biopsy should be considered if elevations persist beyond discontinuation of the drug.
Nicotinic acid should be used with caution in patients who consume substantial quantities of alcohol and/or have a past history of liver disease. Active liver diseases or unexplained transaminase elevations are contraindications to the use of nicotinic acid.
SPL UNCLASSIFIED SECTION
Rare cases of rhabdomyolysis have been associated with concomitant administration of lipid-altering doses of nicotinic acid and HMG-CoA reductase inhibitors. Physicians contemplating combined therapy with HMG-CoA reductase inhibitors and nicotinic acid should carefully weigh the potential benefits and risks and should carefully monitor patients for any signs and symptoms of muscle pain, tenderness, or weakness, particularly during the initial months of therapy and during any periods of upward dosage titration of either drug. Periodic serum creatine phosphokinase (CPK) and potassium determinations should be considered in such situations, but there is no assurance that such monitoring will prevent the occurrence of severe myopathy.
Before instituting therapy with nicotinic acid, an attempt should be made to control hyperlipidemia with appropriate diet, exercise, and weight reduction in obese patients, and to treat other underlying medical problems.
Patients with a past history of jaundice, hepatobiliary disease, or peptic ulcer should be observed closely during nicotinic acid therapy. Frequent monitoring of liver function tests and blood glucose should be performed to ascertain that the drug is producing no adverse effects on these organ systems. Diabetic patients may experience a dose-related rise in glucose intolerance, the clinical significance of which is unclear. Diabetic or potentially diabetic patients should be observed closely. Adjustment of diet and/or hypoglycemic therapy may be necessary.
Caution should also be used when nicotinic acid is used in patients with unstable angina or in the acute phase of myocardial infarction, particularly when such patients are also receiving vasoactive drugs such as nitrates, calcium channel blockers, or adrenergic blocking agents.
Elevated uric acid levels have occurred with nicotinic acid therapy, therefore use with caution in patients predisposed to gout.
HMG-CoA Reductase Inhibitors : See
Antihypertensive Therapy : Nicotinic acid may potentiate the effects of ganglionic blocking agents and vasoactive drugs resulting in postural hypotension.
Aspirin : Concomitant aspirin may decrease the metabolic clearance of nicotinic acid. The clinical relevance of this finding is unclear.
Other : Concomitant alcohol or hot drinks may increase the side effects of flushing and pruritus and should be avoided at the time of drug ingestion.
Carcinogenesis, Mutagenesis, Impairment of Fertility
Nicotinic acid administered to mice for a lifetime as a 1% solution in drinking water was not carcinogenic. The mice in this study received approximately 6-8 times a human dose of 3000 milligrams/day as determined on a milligram/square meter basis. Nicotinic acid was negative for mutagenicity in the Ames test. No studies on impairment of fertility have been performed.
Pregnancy Category C.
Animal reproduction studies have not been conducted with nicotinic acid. It is also not known whether nicotinic acid at doses typically used for lipid disorders can cause fetal harm when administered to pregnant women or whether it can affect reproductive capacity. If a woman receiving nicotinic acid for primary hypercholesterolemia becomes pregnant, the drug should be discontinued. If a woman being treated with nicotinic acid for hypertriglyceridemia (Types IV or V) conceives, the benefits and risks of continued drug therapy should be assessed on an individual basis.
It is not known whether this drug is excreted in human milk. Because many drugs are excreted in human milk and because of the potential for serious adverse reactions in nursing infants from lipid-altering doses of nicotinic acid, a decision should be made whether to discontinue nursing or to discontinue the drug, taking into account the importance of the drug to the mother.
Safety and effectiveness in children and adolescents have not been established.
Cardiovascular : Atrial fibrillation and other cardiac arrhythmias, orthostasis, hypotension.
Gastrointestinal : Dyspepsia, vomiting, diarrhea, peptic ulceration, jaundice, abnormal liver function tests.
Skin : Mild to severe cutaneous flushing, pruritus, hyperpigmentation, acanthosis nigricans, dry skin.
Metabolic : Decreased glucose tolerance, hyperuricemia, gout.
Eye : Toxic amblyopia, cystoid macular edema.
Nervous System / Psychiatric : Headache.
Supportive measures should be undertaken in the event of an overdose.
DOSAGE AND ADMINISTRATION
The usual adult dosage of nicotinic acid is 1 to 2 grams two or three times a day. Doses should be individualized according to the patient's response. Start with one-half tablet as a single daily dose following the evening meal. The frequency of dosing and total daily dose can be increased every four to seven days until the desired LDL cholesterol and/or triglyceride level is achieved or the first-level therapeutic dose of 1.5 to 2 grams/day is reached. If the patient's hyperlipidemia is not adequately controlled after 2 months at this level, the dosage can then be increased at two to four week intervals to 3 grams/day (1 gram three times per day). In patients with marked lipid abnormalities, a higher dose is occasionally required, but generally should not exceed 6 grams/day.
Flushing of the skin appears frequently and can be minimized by pretreatment with aspirin or non-steroidal anti-inflammatory drugs. Tolerance to this flushing develops rapidly over the course of several weeks. Flushing, pruritus, and gastrointestinal distress are also greatly reduced by slowly increasing the dose of nicotinic acid and avoiding administration on an empty stomach.
Sustained-release (modified-release, timed-release) nicotinic acid preparations should not be substituted for equivalent doses of immediate-release (crystalline) nicotinic acid.
Niacin ® (Niacin Tablets, USP) 500 mg.
Each tablet is a white, capsule-shaped, scored, uncoated tablet, debossed “US” to the left and “67” to the right of the score, with “500” strength on the unscored side.
Niacin® is available in bottles of 100 tablets (NDC 0245-0067-11).
Dispense in a tight container as defined in the USP, with a child-resistant closure.
Store at controlled room temperature, 15-30°C (59-86°F).
UPSHER-SMITH LABORATORIES, INC.
Minneapolis, MN 55447
PRINCIPAL DISPLAY PANEL - 500 mg Bottle Label
Niacin Tablets, USP
Niacin pharmaceutical active ingredients containing related brand and generic drugs:
Active ingredient is the part of the drug or medicine which is biologically active. This portion of the drug is responsible for the main action of the drug which is intended to cure or reduce the symptom or disease. The other portions of the drug which are inactive are called excipients; there role is to act as vehicle or binder. In contrast to active ingredient, the inactive ingredient's role is not significant in the cure or treatment of the disease. There can be one or more active ingredients in a drug.
Niacin available forms, composition, doses:
Form of the medicine is the form in which the medicine is marketed in the market, for example, a medicine X can be in the form of capsule or the form of chewable tablet or the form of tablet. Sometimes same medicine can be available as injection form. Each medicine cannot be in all forms but can be marketed in 1, 2, or 3 forms which the pharmaceutical company decided based on various background research results.
Composition is the list of ingredients which combinedly form a medicine. Both active ingredients and inactive ingredients form the composition. The active ingredient gives the desired therapeutic effect whereas the inactive ingredient helps in making the medicine stable.
Doses are various strengths of the medicine like 10mg, 20mg, 30mg and so on. Each medicine comes in various doses which is decided by the manufacturer, that is, pharmaceutical company. The dose is decided on the severity of the symptom or disease.
Niacin destination | category:
Destination is defined as the organism to which the drug or medicine is targeted. For most of the drugs what we discuss, human is the drug destination.
Drug category can be defined as major classification of the drug. For example, an antihistaminic or an antipyretic or anti anginal or pain killer, anti-inflammatory or so.
Niacin Anatomical Therapeutic Chemical codes:
A medicine is classified depending on the organ or system it acts [Anatomical], based on what result it gives on what disease, symptom [Therapeutical], based on chemical composition [Chemical]. It is called as ATC code. The code is based on Active ingredients of the medicine. A medicine can have different codes as sometimes it acts on different organs for different indications. Same way, different brands with same active ingredients and same indications can have same ATC code.
Niacin pharmaceutical companies:
Pharmaceutical companies are drug manufacturing companies that help in complete development of the drug from the background research to formation, clinical trials, release of the drug into the market and marketing of the drug.
Researchers are the persons who are responsible for the scientific research and is responsible for all the background clinical trials that resulted in the development of the drug.
Frequently asked QuestionsCan i drive or operate heavy machine after consuming Niacin?
Depending on the reaction of the Niacin after taken, if you are feeling dizziness, drowsiness or any weakness as a reaction on your body, Then consider Niacin not safe to drive or operate heavy machine after consumption. Meaning that, do not drive or operate heavy duty machines after taking the capsule if the capsule has a strange reaction on your body like dizziness, drowsiness. As prescribed by a pharmacist, it is dangerous to take alcohol while taking medicines as it exposed patients to drowsiness and health risk. Please take note of such effect most especially when taking Primosa capsule. It's advisable to consult your doctor on time for a proper recommendation and medical consultations.Is Niacin addictive or habit forming?
Medicines are not designed with the mind of creating an addiction or abuse on the health of the users. Addictive Medicine is categorically called Controlled substances by the government. For instance, Schedule H or X in India and schedule II-V in the US are controlled substances.
Please consult the medicine instruction manual on how to use and ensure it is not a controlled substance.In conclusion, self medication is a killer to your health. Consult your doctor for a proper prescription, recommendation, and guidiance.
ReviewsDrugs.com conducted a study on Niacin, and the result of the survey is set out below. It is noteworthy that the product of the survey is based on the perception and impressions of the visitors of the website as well as the views of Niacin consumers. We, as a result of this, advice that you do not base your therapeutic or medical decisions on this result, but rather consult your certified medical experts for their recommendations.
Two visitors reported dosesWhat is the dose of Niacin drug you are taking?
According to the survey conducted among sDrugs.com website users, the maximum number of people are using the following dose 11-50mg. Few medications come in only one or two doses. Few are specific for adult dose and child dose. The dose of the medicine given to the patient depends on the severity of the symptom/disease. There can be dose adjustments made by the doctor, based on the progression of the disease. Follow-up is important.
The information was verified by Dr. Arunabha Ray, MD Pharmacology