Niaspan Information
Niaspan (Niacin) Indications And Usage
Therapy with lipid-altering agents should be only one component of multiple risk factor intervention in individuals at significantly increased risk for atherosclerotic vascular disease due to hyperlipidemia. Niacin therapy is indicated as an adjunct to diet when the response to a diet restricted in saturated fat and cholesterol and other nonpharmacologic measures alone has been inadequate.
No incremental benefit of Niaspan (Niacin) coadministered with simvastatin or lovastatin on cardiovascular morbidity and mortality over and above that demonstrated for niacin, simvastatin, or lovastatin monotherapy has been established.
Niaspan (Niacin) Dosage And Administration
Niaspan (Niacin) should be taken at bedtime, after a low-fat snack, and doses should be individualized according to patient response. Therapy with Niaspan (Niacin) must be initiated at 500 mg at bedtime in order to reduce the incidence and severity of side effects which may occur during early therapy. The recommended dose escalation is shown in below.
The daily dosage of Niaspan (Niacin) should not be increased by more than 500 mg in any 4–week period. The recommended maintenance dose is 1000 mg (two 500 mg tablets or one 1000 mg tablet) to 2000 mg (two 1000 mg tablets or four 500 mg tablets) once daily at bedtime. Doses greater than 2000 mg daily are not recommended. Women may respond at lower Niaspan (Niacin) doses than men
Single-dose bioavailability studies have demonstrated that two of the 500 mg and one of the 1000 mg tablet strengths are interchangeable but three of the 500 mg and two of the 750 mg tablet strengths are not interchangeable.
If lipid response to Niaspan (Niacin) alone is insufficient or if higher doses of Niaspan (Niacin) are not well tolerated, some patients may benefit from combination therapy with a bile acid binding resin or statin , below and .
Flushing of the skin may be reduced in frequency or severity by pretreatment with aspirin (up to the recommended dose of 325 mg taken 30 minutes prior to Niaspan (Niacin) dose). 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 niacin and avoiding administration on an empty stomach. Concomitant alcoholic, hot drinks or spicy foods may increase the side effects of flushing and pruritus and should be avoided around the time of Niaspan (Niacin) ingestion.
Equivalent doses of Niaspan (Niacin) should not be substituted for sustained-release (modified-release, timed-release) niacin preparations or immediate-release (crystalline) niacin . Patients previously receiving other niacin products should be started with the recommended Niaspan (Niacin) titration schedule (see ), and the dose should subsequently be individualized based on patient response.
If Niaspan (Niacin) therapy is discontinued for an extended period, reinstitution of therapy should include a titration phase (see ).
Niaspan (Niacin) tablets should be taken whole and should not be broken, crushed or chewed before swallowing.
Patients already receiving a stable dose of lovastatin or simvastatin who require further TG-lowering or HDL-raising (e.g., to achieve NCEP non-HDL-C goals), may receive concomitant dosage titration with Niaspan (Niacin) per Niaspan (Niacin) recommended initial titration schedule . For patients already receiving a stable dose of Niaspan (Niacin) who require further LDL-lowering (e.g., to achieve NCEP LDL-C goals), the usual recommended starting dose of lovastatin and simvastatin is 20 mg once a day. Dose adjustments should be made at intervals of 4 weeks or more. Combination therapy with Niaspan (Niacin) and lovastatin or Niaspan (Niacin) and simvastatin should not exceed doses of 2000 mg Niaspan (Niacin) and 40 mg lovastatin or simvastatin daily.
Use of Niaspan (Niacin) in patients with renal or hepatic impairment has not been studied. Niaspan (Niacin) is contraindicated in patients with significant or unexplained hepatic dysfunction. Niaspan (Niacin) should be used with caution in patients with renal impairment .
Niaspan (Niacin) Contraindications
Niaspan (Niacin) is contraindicated in the following conditions:
Niaspan (Niacin) Warnings And Precautions
Caution should also be used when Niaspan (Niacin) is used in patients with unstable angina or in the acute phase of an MI, particularly when such patients are also receiving vasoactive drugs such as nitrates, calcium channel blockers, or adrenergic blocking agents.
Niacin is rapidly metabolized by the liver, and excreted through the kidneys. Niaspan (Niacin) is contraindicated in patients with significant or unexplained hepatic impairment and should be used with caution in patients with renal impairment. Patients with a past history of jaundice, hepatobiliary disease, or peptic ulcer should be observed closely during Niaspan (Niacin) therapy.
Niaspan (Niacin) Adverse Reactions
Because clinical studies are conducted under widely varying conditions, adverse reaction rates observed in the clinical studies of a drug cannot be directly compared to rates in the clinical studies of another drug and may not reflect the rates observed in practice.
In the placebo-controlled clinical trials database of 402 patients (age range 21-75 years, 33% women, 89% Caucasians, 7% Blacks, 3% Hispanics, 1% Asians) with a median treatment duration of 16 weeks, 16% of patients on Niaspan (Niacin) and 4% of patients on placebo discontinued due to adverse reactions. The most common adverse reactions in the group of patients treated with Niaspan (Niacin) that led to treatment discontinuation and occurred at a rate greater than placebo were flushing (6% vs. 0%), rash (2% vs. 0%), diarrhea (2% vs. 0%), nausea (1% vs. 0%), and vomiting (1% vs. 0%). The most commonly reported adverse reactions (incidence >5% and greater than placebo) in the Niaspan (Niacin) controlled clinical trial database of 402 patients were flushing, diarrhea, nausea, vomiting, increased cough and pruritus.
In the placebo-controlled clinical trials, flushing episodes (i.e., warmth, redness, itching and/or tingling) were the most common treatment-emergent adverse reactions (reported by as many as 88% of patients) for Niaspan (Niacin) . Spontaneous reports suggest that flushing may also be accompanied by symptoms of dizziness, tachycardia, palpitations, shortness of breath, sweating, burning sensation/skin burning sensation, chills, and/or edema, which in rare cases may lead to syncope. In pivotal studies, 6% (14/245) of Niaspan (Niacin) patients discontinued due to flushing. In comparisons of immediate-release (IR) niacin and Niaspan (Niacin) , although the proportion of patients who flushed was similar, fewer flushing episodes were reported by patients who received Niaspan (Niacin) . Following 4 weeks of maintenance therapy at daily doses of 1500 mg, the incidence of flushing over the 4-week period averaged 8.6 events per patient for IR niacin versus 1.9 following Niaspan (Niacin) .
Other adverse reactions occurring in ≥5% of patients treated with Niaspan (Niacin) and at an incidence greater than placebo are shown in below.
In general, the incidence of adverse events was higher in women compared to men.
Because the below reactions are reported voluntarily from a population of uncertain size, it is generally not possible to reliably estimate their frequency or establish a causal relationship to drug exposure.
The following additional adverse reactions have been identified during post-approval use of Niaspan (Niacin) :
Hypersensitivity reactions, including anaphylaxis, angioedema, urticaria, flushing, dyspnea, tongue edema, larynx edema, face edema, peripheral edema, laryngismus, and vesiculobullous rash; maculopapular rash; dry skin; tachycardia; palpitations; atrial fibrillation; other cardiac arrhythmias; syncope; hypotension; postural hypotension; blurred vision; macular edema; peptic ulcers; eructation; flatulence; hepatitis; jaundice; decreased glucose tolerance; gout; myalgia; myopathy; dizziness; insomnia; asthenia; nervousness; paresthesia; dyspnea; sweating; burning sensation/skin burning sensation; skin discoloration, and migraine.
Clinical Laboratory Abnormalities
Niaspan (Niacin) Use In Specific Populations
Pregnancy Category C.
Animal reproduction studies have not been conducted with niacin or with Niaspan (Niacin) . It is also not known whether niacin 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 niacin for primary hyperlipidemia becomes pregnant, the drug should be discontinued. If a woman being treated with niacin for hypertriglyceridemia conceives, the benefits and risks of continued therapy should be assessed on an individual basis.
All statins are contraindicated in pregnant and nursing women. When Niaspan (Niacin) is administered with a statin in a woman of childbearing potential, refer to the pregnancy category and product labeling for the statin.
Niaspan (Niacin) Overdosage
Supportive measures should be undertaken in the event of an overdose.
Niaspan (Niacin) Description
Niaspan (Niacin) (niacin tablet, film-coated extended-release), contains niacin, which at therapeutic doses is an antihyperlipidemic agent. Niacin (nicotinic acid, or 3-pyridinecarboxylic acid) is a white, crystalline powder, very soluble in water, with the following structural formula:
Niaspan (Niacin) is an unscored, medium-orange, film-coated tablet for oral administration and is available in three tablet strengths containing 500, 750, and 1000 mg niacin. Niaspan (Niacin) tablets also contain the inactive ingredients hypromellose, povidone, stearic acid, and polyethylene glycol, and the following coloring agents: FD&C yellow #6/sunset yellow FCF Aluminum Lake, synthetic red and yellow iron oxides, and titanium dioxide.
Niaspan (Niacin) Clinical Pharmacology
Niacin functions in the body after conversion to nicotinamide adenine dinucleotide (NAD) in the NAD coenzyme system. Niacin (but not nicotinamide) in gram doses reduces total cholesterol (TC), low density lipoprotein cholesterol (LDL-C), and triglycerides (TG), and increases high-density lipoprotein cholesterol (HDL-C). The magnitude of individual lipid and lipoprotein responses may be influenced by the severity and type of underlying lipid abnormality. 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 HDL:HDL ratio, and an elevation in lipoprotein A-I (Lp A-I, an HDL-C particle containing only Apo A-I). Niacin treatment also decreases serum levels of apolipoprotein B-100 (Apo B), the major protein component of the very low-density lipoprotein (VLDL) and LDL fractions, and of Lp(a), a variant form of LDL independently associated with coronary risk. In addition, preliminary reports suggest that niacin causes favorable LDL particle size transformations, although the clinical relevance of this effect requires further investigation. The effect of niacin-induced changes in lipids/proteins on cardiovascular morbidity or mortality in individuals without preexisting coronary disease has not been established.
A variety of clinical studies have demonstrated that elevated levels of TC, LDL-C, and Apo B promote human atherosclerosis. Similarly, decreased levels of HDL-C are associated with the development of atherosclerosis. Epidemiological investigations have established that cardiovascular morbidity and mortality vary directly with the level of Total-C and LDL-C, and inversely with the level of HDL-C.
Like LDL, cholesterol-enriched triglyceride-rich lipoproteins, including VLDL, intermediate-density lipoprotein (IDL), and their remnants, can also promote atherosclerosis. Elevated plasma TG are frequently found in a triad with low HDL-C levels and small LDL particles, as well as in association with non-lipid metabolic risk factors for coronary heart disease (CHD). As such, total plasma TG has not consistently been shown to be an independent risk factor for CHD. Furthermore, the independent effect of raising HDL-C or lowering TG on the risk of coronary and cardiovascular morbidity and mortality has not been determined.
Absorption
Due to extensive and saturable first-pass metabolism, niacin concentrations in the general circulation are dose dependent and highly variable. Time to reach the maximum niacin plasma concentrations was about 5 hours following Niaspan (Niacin) . To reduce the risk of gastrointestinal (GI) upset, administration of Niaspan (Niacin) with a low-fat meal or snack is recommended.
Single-dose bioavailability studies have demonstrated that the 500 mg and 1000 mg tablet strengths are dosage form equivalent but the 500 mg and 750 mg tablet strengths are not dosage form equivalent.
Metabolism
The pharmacokinetic profile of niacin is complicated due to extensive first-pass metabolism that is dose-rate specific and, at the doses used to treat dyslipidemia, saturable. In humans, one pathway is through a simple conjugation step with glycine to form nicotinuric acid (NUA). NUA is then excreted in the urine, although there may be a small amount of reversible metabolism back to niacin. The other pathway results in the formation of nicotinamide adenine dinucleotide (NAD). It is unclear whether nicotinamide is formed as a precursor to, or following the synthesis of, NAD. Nicotinamide is further metabolized to at least N-methylnicotinamide (MNA) and nicotinamide-N-oxide (NNO). MNA is further metabolized to two other compounds, N-methyl-2-pyridone-5-carboxamide (2PY) and N-methyl-4-pyridone-5-carboxamide (4PY). The formation of 2PY appears to predominate over 4PY in humans. At the doses used to treat hyperlipidemia, these metabolic pathways are saturable, which explains the nonlinear relationship between niacin dose and plasma concentrations following multiple-dose Niaspan (Niacin) administration.
Nicotinamide does not have hypolipidemic activity; the activity of the other metabolites is unknown.
Elimination
Following single and multiple doses, approximately 60 to 76% of the niacin dose administered as Niaspan (Niacin) was recovered in urine as niacin and metabolites; up to 12% was recovered as unchanged niacin after multiple dosing. The ratio of metabolites recovered in the urine was dependent on the dose administered.
Pediatric Use
No pharmacokinetic studies have been performed in this population (≤16 years) .
Geriatric Use
No pharmacokinetic studies have been performed in this population (> 65 years) .
Renal Impairment
No pharmacokinetic studies have been performed in this population. Niaspan (Niacin) should be used with caution in patients with renal disease .
Hepatic Impairment
No pharmacokinetic studies have been performed in this population. Active liver disease, unexplained transaminase elevations and significant or unexplained hepatic dysfunction are contraindications to the use of Niaspan (Niacin) .
Gender
Steady-state plasma concentrations of niacin and metabolites after administration of Niaspan (Niacin) are generally higher in women than in men, with the magnitude of the difference varying with dose and metabolite. This gender differences observed in plasma levels of niacin and its metabolites may be due to gender-specific differences in metabolic rate or volume of distribution. Recovery of niacin and metabolites in urine, however, is generally similar for men and women, indicating that absorption is similar for both genders .
Drug interactions
Fluvastatin
Niacin did not affect fluvastatin pharmacokinetics
Lovastatin
When Niaspan (Niacin) 2000 mg and lovastatin 40 mg were co-administered, Niaspan (Niacin) increased lovastatin C and AUC by 2% and 14%, respectively, and decreased lovastatin acid C and AUC by 22% and 2%, respectively. Lovastatin reduced Niaspan (Niacin) bioavailability by 2-3% .
Simvastatin
When Niaspan (Niacin) 2000 mg and simvastatin 40 mg were co-administered, Niaspan (Niacin) increased simvastatin C and AUC by 1% and 9%, respectively, and simvastatin acid C and AUC by 2% and 18%, respectively. Simvastatin reduced Niaspan (Niacin) bioavailability by 2% .
Bile Acid Sequestrants
An study was carried out investigating the niacin-binding capacity of colestipol and cholestyramine. About 98% of available niacin was bound to colestipol, with 10 to 30% binding to cholestyramine .
Niaspan (Niacin) Clinical Studies
The role of LDL-C in atherogenesis is supported by pathological observations, clinical studies, and many animal experiments. Observational epidemiological studies have clearly established that high TC or LDL-C and low HDL-C are risk factors for CHD. Additionally, elevated levels of Lp(a) have been shown to be independently associated with CHD risk.
Niacin’s ability to reduce mortality and the risk of definite, nonfatal myocardial infarction (MI) has been assessed in long-term studies. The Coronary Drug Project, completed in 1975, was designed to assess the safety and efficacy of niacin and other lipid-altering drugs in men 30 to 64 years old with a history of MI. Over an observation period of 5 years, niacin treatment was associated with a statistically significant reduction in nonfatal, recurrent MI. 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 (
The Cholesterol-Lowering Atherosclerosis Study (CLAS) was a randomized, placebo-controlled, angiographic trial testing combined colestipol and niacin therapy in 162 non-smoking males with previous coronary bypass surgery. The primary, per-subject cardiac endpoint was global coronary artery change score. After 2 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 (
The Familial Atherosclerosis Treatment Study (FATS) in 146 men ages 62 and younger with Apo 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 arteriography. Patients were given dietary counseling and randomized to treatment with either conventional therapy with double placebo (or placebo plus colestipol if the LDL-C was elevated); lovastatin plus colestipol; or niacin 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; regression was the only change in 11%. In contrast, progression (as the only change) was seen in only 25% in the niacin plus colestipol group, while regression was observed in 39%. Though not an original endpoint of the trial, clinical events (death, MI, or revascularization for worsening angina) occurred in 10 of 52 patients who received conventional therapy, compared with 2 of 48 who received niacin plus colestipol.
The Harvard Atherosclerosis Reversibility Project (HARP) was a randomized placebo-controlled, 2.5-year study of the effect of a stepped-care antihyperlipidemic drug regimen on 91 patients (80 men and 11 women) with CHD and average baseline TC levels less than 250 mg/dL and ratios of TC to HDL-C greater than 4.0. Drug treatment consisted of an HMG-CoA reductase inhibitor administered alone as initial therapy followed by addition of varying dosages of either a slow-release nicotinic acid, cholestyramine, or gemfibrozil. Addition of nicotinic acid to the HMG-CoA reductase inhibitor resulted in further statistically significant mean reductions in TC, LDL-C, and TG, as well as a further increase in HDL-C in a majority of patients (40 of 44 patients). The ratios of TC to HDL-C and LDL-C to HDL-C were also significantly reduced by this combination drug regimen .
Table 3
In a double-blind, multi-center, forced dose-escalation study, monthly 500 mg increases in Niaspan (Niacin) dose resulted in incremental reductions of approximately 5% in LDL-C and Apo B levels in the daily dose range of 500 mg through 2000 mg (). Women again tended to have a greater response to Niaspan (Niacin) than men (see , below).
Pooled results for major lipids from these three placebo-controlled studies are shown below ().
Gender Effect:
Table 6
Other Patient Populations:
Table 7
At Niaspan (Niacin) 2000 mg/day, median changes from baseline (25th, 75th percentiles) for LDL-C, HDL-C, and TG were -3% (-14, +12%), +27% (+13, +38%), and -33% (-50, -19%), respectively.
Combination Niaspan (Niacin) and Lovastatin Study: In a multi-center, randomized, double-blind, parallel, 28-week study, a combination tablet of Niaspan (Niacin) and lovastatin was compared to each individual component in patients with Type IIa and IIb hyperlipidemia. Using a forced dose-escalation study design, patients received each dose for at least 4 weeks. Patients randomized to treatment with the combination tablet of Niaspan (Niacin) and lovastatin initially received 500 mg/20 mg (expressed as mg of niacin/mg of lovastatin) once daily before bedtime. The dose was increased by 500 mg at 4-week intervals (based on the Niaspan (Niacin) component) to a maximum dose of 1000 mg/20 mg in one-half of the patients and 2000 mg/40 mg in the other half. The Niaspan (Niacin) monotherapy group underwent a similar titration from 500 mg to 2000 mg. The patients randomized to lovastatin monotherapy received 20 mg for 12 weeks titrated to 40 mg for up to 16 weeks. Up to a third of the patients randomized to the combination tablet of Niaspan (Niacin) and lovastatin or Niaspan (Niacin) monotherapy discontinued prior to Week 28. Results from this study showed that combination therapy decreased LDL-C, TG and Lp(a), and increased HDL-C in a dose-dependent fashion (Tables 8, 9, 10, and 11). Results from this study for LDL-C mean percent change from baseline (the primary efficacy variable) showed that:
The LDL-C results are summarized in .
Combination therapy achieved significantly greater HDL-raising compared to lovastatin and Niaspan (Niacin) monotherapy at all doses ().
In addition, combination therapy achieved significantly greater TG lowering at doses of 1000 mg/20mg or greater compared to lovastatin and Niaspan (Niacin) monotherapy ().
The Lp(a)-lowering effects of combination therapy and Niaspan (Niacin) monotherapy were similar, and both were superior to lovastatin (). The independent effect of lowering Lp(a) with Niaspan (Niacin) or combination therapy on the risk of coronary and cardiovascular morbidity and mortality has not been determined.
In a double-blind, randomized, multicenter, multi-national, active-controlled, 24-week study, the lipid effects of a combination tablet of Niaspan (Niacin) and simvastatin were compared to simvastatin 20 mg and 80 mg in 641 patients with type II hyperlipidemia or mixed dyslipidemia. Following a lipid qualification phase, patients were eligible to enter one of two treatment groups. In Group A, patients on simvastatin 20 mg monotherapy, with elevated non-HDL levels and LDL-C levels at goal per the NCEP guidelines, were randomized to one of three treatment arms: combination tablet of Niaspan (Niacin) and simvastatin 1000/20 mg, combination tablet of Niaspan (Niacin) and simvastatin 2000/20 mg, or simvastatin 20 mg. In Group B, patients on simvastatin 40 mg monotherapy, with elevated non-HDL levels per the NCEP guidelines regardless of attainment of LDL-C goals, were randomized to one of three treatment arms: combination tablet of Niaspan (Niacin) and simvastatin 1000/40 mg, combination tablet of Niaspan (Niacin) and simvastatin 2000/40 mg, or simvastatin 80 mg. Therapy was initiated at the 500 mg dose of combination tablet of Niaspan (Niacin) and simvastatin and increased by 500 mg every four weeks. Thus patients were titrated to the 1000 mg dose of combination tablet of Niaspan (Niacin) and simvastatin after four weeks and to the 2000 mg dose of combination tablet of Niaspan (Niacin) and simvastatin after 12 weeks. All patients randomized to simvastatin monotherapy received 50 mg immediate-release niacin daily in an attempt to keep the study from becoming unblinded due to flushing in the combination tablet of Niaspan (Niacin) and simvastatin groups. Patients were instructed to take one 325 mg aspirin or 200 mg ibuprofen 30 minutes prior to taking the double-blind medication to help minimize flushing effects.
In Group A, the primary efficacy analysis was a comparison of the mean percent change in non-HDL levels between the combination tablet of Niaspan (Niacin) and simvastatin 2000/20 mg and simvastatin 20 mg groups, and if statistically significant, then a comparison was conducted between the combination tablet of Niaspan (Niacin) and simvastatin 1000/20 mg and simvastatin 20 mg groups. In Group B, the primary efficacy analysis was a determination of whether the mean percent change in non-HDL in the combination tablet of Niaspan (Niacin) and simvastatin 2000/40 mg group was non-inferior to the mean percent change in the simvastatin 80 mg group, and if so, whether the mean percent change in non-HDL in the combination tablet of Niaspan (Niacin) and simvastatin 1000/40 mg group was non-inferior to the mean percent change in the simvastatin 80 mg group.
In Group A, the non-HDL-C lowering with combination tablet of Niaspan (Niacin) and simvastatin 2000/20 and combination tablet of Niaspan (Niacin) and simvastatin 1000/20 was statistically significantly greater than that achieved with simvastatin 20 mg after 24 weeks (
The combination tablet of Niaspan (Niacin) and simvastatin was not superior to simvastatin in lowering LDL-C in either Group A or Group B. However, the combination tablet of Niaspan (Niacin) and simvastatin was superior to simvastatin in both groups in lowering TG and raising HDL (Tables and ).
Niaspan (Niacin) How Supplied/storage And Handling
Niaspan (Niacin) tablets are supplied as unscored, medium-orange, film-coated, capsule-shaped (containing 500 or 750 mg of niacin) or oval shaped (containing 1000 mg of niacin) tablets, in an extended-release formulation. Tablets are printed with the Abbott ‘A’ logo and the tablet strength (500, 750 or 1000). Tablets are supplied in bottles of 90 as shown below.
500 mg tablets:bottles of 90 - NDC# 21695-852–90
1000 mg tablets:bottles of 90 - NDC# 21695-865-90
Storage: Store at room temperature 20° to 25°C (68° to 77°F).
Niaspan (Niacin) Patient Information
Read this information carefully before you start taking Niaspan (Niacin) and each time you get a refill. There may be new information. This information does not take the place of talking with your doctor about your medical condition or your treatment.
Niaspan (Niacin) is a prescription medicine used with diet and exercise to increase the good cholesterol (HDL) and lower the bad cholesterol (LDL) and fats (triglycerides) in your blood.
It is not known if Niaspan (Niacin) is safe and effective in children 16 years of age and under.
Know the medicines you take. Keep a list of them to show your doctor and pharmacist when you get a new medicine.
Call your doctor right away if you have any of the side effects listed above.
The most common side effects of Niaspan (Niacin) include:
Flushing does not always happen. If it does, it is usually within 2 to 4 hours after taking a dose of Niaspan (Niacin) . Flushing may last for a few hours. Flushing is more likely to happen when you first start taking Niaspan (Niacin) or when your dose of Niaspan (Niacin) is increased. Flushing may get better after several weeks.
If you wake up at night because of flushing, get up slowly, especially if you:
To lower your chance of flushing:
People with high cholesterol and heart disease are at risk for a heart attack. Symptoms of a heart attack may be different from a flushing reaction from Niaspan (Niacin) .
The chest pain you have with a heart attack may feel like uncomfortable pressure, squeezing, fullness or pain that lasts more than a few minutes, or that goes away and comes back. Heart attacks may be sudden and intense, but often start slowly, with mild pain or discomfort.
Call your doctor right away if you have any symptoms of a heart attack.
Tell your doctor if you have any side effect that bothers you or does not go away.
These are not all the possible side effects of Niaspan (Niacin) . For more information, ask your doctor or pharmacist.
Call your doctor for medical advice about side effects. You may report side effects to FDA at 1-800-FDA-1088.
Medicines are sometimes prescribed for purposes other than those listed in a patient information leaflet. Do not use Niaspan (Niacin) for a condition for which it was not prescribed. Do not give Niaspan (Niacin) to other people, even if they have the same symptoms that you have. It may harm them.
This leaflet summarizes the most important information about Niaspan (Niacin) . If you would like more information, talk with your doctor. You can ask your pharmacist or doctor for information about Niaspan (Niacin) that is written for health professionals.
For more information, go to www.Niaspan (Niacin) .com or call Abbott Medical Information at 1-800-633-9110.
niacin
hypromellose, povidone, stearic acid, and polyethylene glycol, and the following coloring agents: FD& C yellow #6/sunset yellow FCF Aluminum Lake, synthetic red and yellow iron oxides, and titanium dioxide.
Manufactured for Abbott Laboratories, North Chicago, IL 60064, U.S.A.
500 mg tablets by Norwich Pharmaceuticals, Inc., Norwich, NY 13815
or 500 mg, 750 mg and 1000 mg tablets
by Abbott Pharmaceuticals PR Ltd., Barceloneta, PR 00617
Revised 11/2010 Abbott Laboratories
Niaspan (Niacin) Principal Display Panel
NDC 21695-852–90
Niaspan (Niacin) ® Niacin Extended-Release Tablets 500mg 90 Tablets RX only
Niaspan (Niacin) Principal Display Panel
NDC 21695-865–90
Niaspan (Niacin) ® Niacin Extended-Release Tablets 1000mg 90 Tablets RX only
