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All about: Advicor

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Generic Name: niacin and lovastatin
Dosage Form: Extended release tablets

Annotated Final Package Insert
Advicor CBE-0 Labeling Supplement:
Additional Safety Information


Advicor Description

Advicor contains niacin extended-release and lovastatin in combination. Lovastatin, an inhibitor of 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase, and niacin are both lipid-altering agents.

Niacin is nicotinic acid, or 3-pyridinecarboxylic acid. Niacin is a white, nonhygroscopic crystalline powder that is very soluble in water, boiling ethanol and propylene glycol. It is insoluble in ethyl ether. The empirical formula of niacin is C6H5NO2 and its molecular weight is 123.11. Niacin has the following structural formula:

Lovastatin is [1S -[1(alpha)(R *), 3(alpha), 7(beta), 8(beta)(2S *, 4S *), 8a(beta)]]-1,2,3, 7,8,8a-hexahydro-3,7-dimethyl-8-[2-(tetrahydro-4-hydroxy-6-oxo-2H-pyran-2-yl) ethyl]-1-naphthalenyl 2-methylbutanoate. Lovastatin is a white, nonhygroscopic crystalline powder that is insoluble in water and sparingly soluble in ethanol, methanol, and acetonitrile. The empirical formula of lovastatin is C24H36O5 and its molecular weight is 404.55. Lovastatin has the following structural formula:

Advicor tablets contain the labeled amount of niacin and lovastatin and have the following inactive ingredients: hypromellose, povidone, stearic acid, polyethylene glycol, titanium dioxide, polysorbate 80.

The individual tablet strengths (expressed in terms of mg niacin/mg lovastatin) contain the following coloring agents:

Advicor 500 mg/20 mg - synthetic red and yellow iron oxides.
Advicor 750 mg/20 mg – FD&C yellow #6 Aluminum Lake.
Advicor 1000 mg/20 mg - synthetic red, yellow, and black iron oxides.
Advicor 1000 mg/40 mg – red iron oxide.

Advicor - Clinical Pharmacology

A variety of clinical studies have demonstrated that elevated levels of total cholesterol (TC), low-density lipoprotein cholesterol (LDL-C), and apolipoprotein B-100 (Apo B) promote human atherosclerosis. Similarly, decreased levels of high-density lipoprotein cholesterol (HDL-C) are associated with the development of atherosclerosis. Epidemiological investigations have established that cardiovascular morbidity and mortality vary directly with the level of TC and LDL-C, and inversely with the level of HDL-C.

Cholesterol-enriched triglyceride-rich lipoproteins, including very low-density lipoproteins (VLDL), intermediate-density lipoproteins (IDL), and their remnants, can also promote atherosclerosis. Elevated plasma triglycerides (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 have not consistently been shown to be an independent risk factor for CHD.

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.

Effects on lipids


Advicor reduces LDL-C, TC, and TG, and increases HDL-C due to the individual actions of niacin and lovastatin. The magnitude of individual lipid and lipoprotein responses may be influenced by the severity and type of underlying lipid abnormality.


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 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). In addition, preliminary reports suggest that niacin causes favorable LDL particle size transformations, although the clinical relevance of this effect is not yet clear.


Lovastatin has been shown to reduce both normal and elevated LDL-C concentrations. Apo B also falls substantially during treatment with lovastatin. Since each LDL-C particle contains one molecule of Apo B, and since little Apo B is found in other lipoproteins, this strongly suggests that lovastatin does not merely cause cholesterol to be lost from LDL-C, but also reduces the concentration of circulating LDL particles. In addition, lovastatin can produce increases of variable magnitude in HDL-C, and modestly reduces VLDL-C and plasma TG. The effects of lovastatin on Lp(a), fibrinogen, and certain other independent biochemical risk markers for coronary heart disease are not well characterized.

Mechanism of Action


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.


Lovastatin is a specific inhibitor of 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase, the enzyme that catalyzes the conversion of HMG-CoA to mevalonate. The conversion of HMG-CoA to mevalonate is an early step in the biosynthetic pathway for cholesterol. Lovastatin is a prodrug and has little, if any, activity until hydrolyzed to its active beta-hydroxyacid form, lovastatin acid. The mechanism of the LDL-lowering effect of lovastatin may involve both reduction of VLDL-C concentration and induction of the LDL receptor, leading to reduced production and/or increased catabolism of LDL-C.


Absorption and Bioavailability


In single-dose studies of Advicor, rate and extent of niacin and lovastatin absorption were bioequivalent under fed conditions to that from NIASPAN® (niacin extended-release tablets) and Mevacor® (lovastatin) tablets, respectively. After administration of two Advicor 1000 mg/20 mg tablets, peak niacin concentrations averaged about 18 mcg/mL and occurred about 5 hours after dosing; about 72% of the niacin dose was absorbed according to the urinary excretion data. Peak lovastatin concentrations averaged about 11 ng/mL and occurred about 2 hours after dosing.

The extent of niacin absorption from Advicor was increased by administration with food. The administration of two Advicor 1000 mg/20 mg tablets under low-fat or high-fat conditions resulted in a 22 to 30% increase in niacin bioavailability relative to dosing under fasting conditions. Lovastatin bioavailability is affected by food. Lovastatin Cmax was increased 48% and 21% after a high- and a low-fat meal, respectively, but the lovastatin AUC was decreased 26% and 24% after a high- and a low-fat meal, respectively, compared to those under fasting conditions.

A relative bioavailability study results indicated that Advicor tablet strengths (i.e., two tablets of 500 mg/20 mg and one tablet of 1000 mg/40 mg) are not interchangeable.


Due to extensive and saturable first-pass metabolism, niacin concentrations in the general circulation are dose dependent and highly variable. Peak steady-state niacin concentrations were 0.6, 4.9, and 15.5 mcg/mL after doses of 1000, 1500, and 2000 mg NIASPAN once daily (given as two 500 mg, two 750 mg, and two 1000 mg tablets, respectively).


Lovastatin appears to be incompletely absorbed after oral administration. Because of extensive hepatic extraction, the amount of lovastatin reaching the systemic circulation as active inhibitors after oral administration is low (<5%) and shows considerable inter-individual variation. Peak concentrations of active and total inhibitors occur within 2 to 4 hours after Mevacor® administration.

Lovastatin absorption appears to be increased by at least 30% by grapefruit juice; however, the effect is dependent on the amount of grapefruit juice consumed and the interval between grapefruit juice and lovastatin ingestion. With a once-a-day dosing regimen, plasma concentrations of total inhibitors over a dosing interval achieved a steady-state between the second and third days of therapy and were about 1.5 times those following a single dose of Mevacor®.



Niacin is less than 20% bound to human serum proteins and distributes into milk. Studies using radiolabeled niacin in mice show that niacin and its metabolites concentrate in the liver, kidney, and adipose tissue.


Both lovastatin and its beta-hydroxyacid metabolite are highly bound (>95%) to human plasma proteins. Distribution of lovastatin or its metabolites into human milk is unknown; however, lovastatin distributes into milk in rats. In animal studies, lovastatin concentrated in the liver, and crossed the blood-brain and placental barriers.



Niacin undergoes rapid and 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, although there may be a small amount of reversible metabolism back to niacin. The other pathway results in the formation of 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.


Lovastatin undergoes extensive first-pass extraction and metabolism by cytochrome P450 3A4 in the liver, its primary site of action. The major active metabolites present in human plasma are the beta-hydroxyacid of lovastatin (lovastatin acid), its 6'-hydroxy derivative, and two additional metabolites.



Niacin is primarily excreted in urine mainly as metabolites. After a single dose of Advicor, at least 60% of the niacin dose was recovered in urine as unchanged niacin and its metabolites. The plasma half-life for lovastatin was about 4.5 hours in single-dose studies.


The plasma half-life for niacin is about 20 to 48 minutes after oral administration and dependent on dose administered. Following multiple oral doses of NIASPAN, up to 12% of the dose was recovered in urine as unchanged niacin depending on dose administered. The ratio of metabolites recovered in the urine was also dependent on the dose administered.


Lovastatin is excreted in urine and bile, based on studies of Mevacor®. Following an oral dose of radiolabeled lovastatin in man, 10% of the dose was excreted in urine and 83% in feces. The latter represents absorbed drug equivalents excreted in bile, as well as any unabsorbed drug.

Special Populations


No pharmacokinetic studies have been conducted in patients with hepatic insufficiency for either niacin or lovastatin (see WARNINGS, Liver Dysfunction).


No information is available on the pharmacokinetics of niacin in patients with renal insufficiency.

In a study of patients with severe renal insufficiency (creatinine clearance 10 to 30 mL/min), the plasma concentrations of total inhibitors after a single dose of lovastatin were approximately two-fold higher than those in healthy volunteers.

Advicor should be used with caution in patients with renal disease.


Plasma concentrations of niacin and metabolites after single- or multiple-dose administration of niacin are generally higher in women than in men, with the magnitude of the difference varying with dose and metabolite. Recovery of niacin and metabolites in urine, however, is generally similar for men and women, indicating similar absorption for both genders. The gender differences observed in plasma niacin and metabolite levels may be due to gender-specific differences in metabolic rate or volume of distribution. Data from clinical trials suggest that women have a greater hypolipidemic response than men at equivalent doses of NIASPAN® and Advicor.

In a multiple-dose study, plasma concentrations of active and total HMG-CoA reductase inhibitors were 20 to 50% higher in women than in men. In two single-dose studies with Advicor, lovastatin concentrations were about 30% higher in women than men, and total HMG-CoA reductase inhibitor concentrations were about 20 to 25% greater in women.

In a multi-center, randomized, double-blind, active-comparator study in patients with Type IIa and IIb hyperlipidemia, Advicor was compared to single-agent treatment (NIASPAN and lovastatin). The treatment effects of Advicor compared to lovastatin and NIASPAN differed for males and females with a significantly larger treatment effect seen for females. The mean percent change from baseline at endpoint for LDL-C, TG, and HDL-C by gender are as follows (Table 1):

Table 1. Mean percent change from baseline at endpoint for LDL-C, HDL-C and TG by gender
Advicor 2000 mg/40 mg NIASPAN 2000 mg Lovastatin 40 mg
LDL-C -47% -34% -12% -9% -31% -31%
HDL-C +33% +24% +22% +15% +3% +7%
TG -48% -35% -25% -15% -15% -23%

Clinical Studies

In a multi-center, randomized, double-blind, parallel, 28-week, active-comparator study in patients with Type IIa and IIb hyperlipidemia, Advicor was compared to each of its components (NIASPAN and lovastatin). Using a forced dose-escalation study design, patients received each dose for at least 4 weeks. Patients randomized to treatment with Advicor initially received 500 mg/20 mg. The dose was increased at 4-week intervals to a maximum of 1000 mg/20 mg in one-half of the patients and 2000 mg/40 mg in the other half. The NIASPAN 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 Advicor or NIASPAN discontinued prior to Week 28. In this study, Advicor decreased LDL-C, TG and Lp(a), and increased HDL-C in a dose-dependent fashion (Tables 2, 3, 4 and 5 below). Results from this study for LDL-C mean percent change from baseline (the primary efficacy variable) showed that:

  1. LDL-lowering with Advicor was significantly greater than that achieved with lovastatin 40 mg only after 28 weeks of titration to a dose of 2000 mg/40 mg (p<.0001)
  2. Advicor at doses of 1000 mg/20 mg or higher achieved greater LDL-lowering than NIASPAN (p<.0001) The LDL-C results are summarized in Table 2.
Table 2. LDL-C mean percent change from baseline

*n = number of patients remaining in the trial at each timepoint

Week Advicor NIASPAN Lovastatin
n* Dose
LDL n* Dose
LDL n* Dose
Baseline 57 - 190.9 mg/dL 61 - 189.7 mg/dL 61 - 185.6 mg/dL
12 47 1000/20 -30% 46 1000 -3% 56 20 -29%
16 45 1000/40 -36% 44 1000 -6% 56 40 -31%
20 42 1500/40 -37% 43 1500 -12% 54 40 -34%
28 42 2000/40 -42% 41 2000 -14% 53 40 -32%

Advicor achieved significantly greater HDL-raising compared to lovastatin and NIASPAN monotherapy at all doses (Table 3).

Table 3. HDL-C mean percent change from baseline

*n = number of patients remaining in the trial at each timepoint

Week Advicor NIASPAN Lovastatin
n* Dose
HDL n* Dose
HDL n* Dose
Baseline 57 - 45 mg/dL 61 - 47 mg/dL 61 - 43 mg/dL
12 47 1000/20 +20% 46 1000 +14% 56 20 +3%
16 45 1000/40 +20% 44 1000 +15% 56 40 +5%
20 42 1500/40 +27% 43 1500 +22% 54 40 +6%
28 42 2000/40 +30% 41 2000 +24% 53 40 +6%

In addition, Advicor achieved significantly greater TG-lowering at doses of 1000 mg/20 mg or greater compared to lovastatin and NIASPAN monotherapy (Table 4).

Table 4. TG median percent change from baseline

*n = number of patients remaining in the trial at each timepoint

Week Advicor NIASPAN Lovastatin
n* Dose
TG n* Dose
TG n* Dose
Baseline 57 - 174 mg/dL 61 - 186 mg/dL 61 - 171 mg/dL
12 47 1000/20 -32% 46 1000 -22% 56 20 -20%
16 45 1000/40 -39% 44 1000 -23% 56 40 -17%
20 42 1500/40 -44% 43 1500 -31% 54 40 -21%
28 42 2000/40 -44% 41 2000 -31% 53 40 -20%

The Lp(a) lowering effects of Advicor and NIASPAN were similar, and both were superior to lovastatin (Table 5). The independent effect of lowering Lp(a) with NIASPAN or Advicor on the risk of coronary and cardiovascular morbidity and mortality has not been determined.

Table 5. Lp(a) median percent change from baseline

*n = number of patients remaining in the trial at each timepoint

Week Advicor NIASPAN Lovastatin
n* Dose
Lp(a) n* Dose
Lp(a) n* Dose
Baseline 57 - 34 mg/dL 61 - 41 mg/dL 60 - 42 mg/dL
12 47 1000/20 -9% 46 1000 -8% 55 20 +8%
16 45 1000/40 -9% 44 1000 -12% 55 40 +8%
20 42 1500/40 -17% 43 1500 -22% 53 40 +6%
28 42 2000/40 -22% 41 2000 -32% 52 40 0%

Advicor Long-Term Study

A total of 814 patients were enrolled in a long-term (52-week), open-label, single-arm study of Advicor. Patients were force dose-titrated to 2000 mg/40 mg over 16 weeks. After titration, patients were maintained on the maximum tolerated dose of Advicor for a total of 52 weeks. Five hundred-fifty (550) patients (68%) completed the study, and fifty-six percent (56%) of all patients were able to maintain a dose of 2000 mg/40 mg for the 52 weeks of treatment. The lipid-altering effects of Advicor peaked after 4 weeks on the maximum tolerated dose, and were maintained for the duration of treatment. These effects were comparable to what was observed in the double-blind study of Advicor (Tables 2-4).

Indications and Usage for Advicor

Advicor is a fixed-dose combination product and is not indicated for initial therapy (see DOSAGE AND ADMINISTRATION). 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 hypercholesterolemia. Initial medical therapy is indicated with a single agent 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 (see also Table 7 and the NCEP treatment guidelines1).

Advicor is indicated for the treatment of primary hypercholesterolemia (heterozygous familial and nonfamilial) and mixed dyslipidemia (Frederickson Types IIa and IIb; Table 6) in:

• Patients treated with lovastatin who require further TG-lowering or HDL-raising who may benefit from having niacin added to their regimen

• Patients treated with niacin who require further LDL-lowering who may benefit from having lovastatin added to their regimen.

Table 6. Classification of Hyperlipoproteinemias
Lipid Elevations
Type Lipoproteins Elevated


TC = total cholesterol; TG = triglycerides; LDL = low-density lipoprotein; VLDL = very low-density lipoprotein; IDL = intermediate-density lipoprotein ↑→ = increased or no change

I (rare) Chylomicrons TG ↑→TC
III (rare) IDL TC/TG -
V (rare) Chylomicrons, VLDL TG ↑→TC

General Recommendations

Prior to initiating therapy with a lipid-lowering agent, 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 TC, HDL-C, and TG. For patients with TG < 400 mg/dL, LDL-C can be estimated using the following equation:

LDL-C = TC – [(0.20 x TG) + HDL-C]

For TG levels > 400 mg/dL, this equation is less accurate and LDL-C concentrations should be determined by ultracentrifugation. Lipid determinations should be performed at intervals of no less than 4 weeks and dosage adjusted according to the patient's response to therapy. The NCEP Treatment Guidelines are summarized in Table 7.

Table 7. NCEP Treatment Guidelines: LDL-C Goals and Cutpoints for Therapeutic Lifestyle Changes and Drug Therapy in Different Risk Categories

CHD, coronary heart disease

†† Some authorities recommend use of LDL-lowering drugs in this category if an LDL-C level of <100 mg/dL cannot be achieved by therapeutic lifestyle changes. Others prefer use of drugs that primarily modify triglycerides and HDL-C, e.g., nicotinic acid or fibrate. Clinical judgement also may call for deferring drug therapy in this subcategory.

††† Almost all people with 0-1 risk factor have 10-year risk <10%; thus, 10-year risk assessment in people with 0-1 risk factor is not necessary.

Risk Category LDL Goal
LDL Level at Which to Initiate Therapeutic Lifestyle Changes
LDL Level at Which to
Consider Drug
Therapy (mg/dL)
risk equivalents
(10-year risk >20%)
<100 ≥100 ≥130
(100-129:drug optional) ††
2+ Risk factors
(10-year risk≤20%)
<130 ≥130 10-year risk 10%-20%: ≥ 130
10-year risk <10%: ≥ 160
   0-1 Risk factor ††† <160 ≥160 ≥190
(160-189:LDL-lowering drug optional)

After the LDL-C goal has been achieved, if the TG is still ≥200 mg/dL, non-HDL-C (TC minus HDL-C) becomes a secondary target of therapy. Non-HDL-C goals are set 30 mg/dL higher than LDL-C goals for each risk category.


Advicor is contraindicated in patients with a known hypersensitivity to niacin, lovastatin or any component of this medication, active liver disease or unexplained persistent elevations in serum transaminases (see WARNINGS), active peptic ulcer disease, or arterial bleeding.

Pregnancy and lactation– Atherosclerosis is a chronic process and the discontinuation of lipid-lowering drugs during pregnancy should have little impact on the outcome of long-term therapy of primary hypercholesterolemia. Moreover, cholesterol and other products of the cholesterol biosynthesis pathway are essential components for fetal development, including synthesis of steroids and cell membranes. Because of the ability of inhibitors of HMG-CoA reductase, such as lovastatin, to decrease the synthesis of cholesterol and possibly other products of the cholesterol biosynthesis pathway, Advicor is contraindicated in women who are pregnant and in lactating mothers. Advicor may cause fetal harm when administered to pregnant women. Advicor should be administered to women of childbearing age only when such patients are highly unlikely to conceive. If the patient becomes pregnant while taking this drug, Advicor should be discontinued immediately and the patient should be apprised of the potential hazard to the fetus (see PRECAUTIONS, Pregnancy).


Advicor should not be substituted for equivalent doses of immediate-release (crystalline) niacin. For patients switching from immediate-release niacin to NIASPAN, therapy with NIASPAN should be initiated with low doses (i.e., 500 mg once daily at bedtime) and the NIASPAN dose should then be titrated to the desired therapeutic response (see DOSAGE AND ADMINISTRATION).

Liver Dysfunction

Cases of severe hepatic toxicity, including fulminant hepatic necrosis, have occurred in patients who have substituted sustained-release (modified-release, timed-release) niacin products for immediate-release (crystalline) niacin at equivalent doses.

Advicor should be used with caution in patients who consume substantial quantities of alcohol and/or have a past history of liver disease. Active liver disease or unexplained transaminase elevations are contraindications to the use of Advicor.

Niacin preparations and lovastatin preparations have been associated with abnormal liver tests. In studies using NIASPAN alone, 0.8% of patients were discontinued for transaminase elevations. In studies using lovastatin alone, 0.2% of patients were discontinued for transaminase elevations.2 In three safety and efficacy studies involving titration to final daily Advicor doses ranging from 500 mg/10 mg to 2500 mg/40 mg, ten of 1028 patients (1.0%) experienced reversible elevations in AST/ALT to more than 3 times the upper limit of normal (ULN). Three of ten elevations occurred at doses outside the recommended dosing limit of 2000 mg/40 mg; no patient receiving 1000 mg/20 mg had 3-fold elevations in AST/ALT.

In clinical studies with Advicor, elevations in transaminases did not appear to be related to treatment duration; elevations in AST and ALT levels did appear to be dose related. Transaminase elevations were reversible upon discontinuation of Advicor.

Liver function tests should be performed on all patients during therapy with Advicor. Serum transaminase levels, including AST and ALT (SGOT and SGPT), should be monitored before treatment begins, every 6 to 12 weeks for the first 6 months, 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, if confirmed, then performed more frequently. If the transaminase levels show evidence of progression, particularly if they rise to 3 times ULN and are persistent, or if they are associated with symptoms of nausea, fever, and/or malaise, the drug should be discontinued.

Skeletal Muscle


Lovastatin and other inhibitors of HMG-CoA reductase occasionally cause myopathy, which is manifested as muscle pain or weakness associated with grossly elevated creatine kinase (> 10 times ULN). Rhabdomyolysis, with or without acute renal failure secondary to myoglobinuria, has been reported rarely and can occur at any time. In a large, long-term, clinical safety and efficacy study (the EXCEL study)3,4 with lovastatin, myopathy occurred in up to 0.2% of patients treated with lovastatin 20 to 80 mg for up to 2 years. When drug treatment was interrupted or discontinued in these patients, muscle symptoms and creatine kinase (CK) increases promptly resolved. The risk of myopathy is increased by concomitant therapy with certain drugs, some of which were excluded by the EXCEL study design.

Potent inhibitors of CYP3A4: The risk of myopathy appears to be increased by high levels of HMG-CoA reductase inhibitory activity in plasma. Lovastatin is metabolized by the cytochrome P450 isoform 3A4. Certain drugs which share this metabolic pathway can raise the plasma levels of lovastatin and may increase the risk of myopathy. These include cyclosporine, itraconazole, ketoconazole a

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