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Mechanism of Action
Lovastatin is a lactone that is readily hydrolyzed in vivo to the corresponding β-hydroxyacid, a strong inhibitor of 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, as well as some of its metabolites, are pharmacologically active in humans. The liver is the primary site of action and the principal site of cholesterol synthesis and LDL clearance.
The involvement of low-density lipoprotein cholesterol (LDL-C) in atherogenesis has been well documented in clinical and pathological studies, as well as in many animal experiments. Epidemiological and clinical studies have established that high LDL-C and low high-density lipoprotein cholesterol (HDL-C) levels are both associated with coronary heart disease. However, the risk of developing coronary heart disease is continuous and graded over the range of cholesterol levels and many coronary events do occur in patients with total cholesterol (Total-C) and LDL-C levels in the lower end of this range.
Altoprev® has been shown to reduce LDL-C, and Total-C. Across all doses studied, treatment with Altoprev® has been shown to result in variable reductions in triglycerides (TG), and variable increases in HDL-C [see Table 6 under Clinical Studies].
Lovastatin Immediate-Release Tablets have been shown to reduce both normal and elevated LDL-C concentrations. LDL is formed from very low-density lipoprotein (VLDL) and is catabolized predominantly by the high-affinity LDL receptor. The mechanism of the LDL-lowering effect of lovastatin Immediate-Release 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. Apolipoprotein B (Apo B) also falls substantially during treatment with lovastatin Immediate-Release. Since each LDL particle contains one molecule of Apo B, and since little Apo B is found in other lipoproteins, this strongly suggests that lovastatin immediate-release does not merely cause cholesterol to be lost from LDL, but also reduces the concentration of circulating LDL particles. In addition, lovastatin immediate-release can produce increases of variable magnitude in HDL-C, and modestly reduces VLDL-C and plasma TG [see Table 7 under Clinical Studies]. The independent effect of raising HDL or lowering TG on the risk of coronary and cardiovascular morbidity and mortality has not been determined. The effects of lovastatin immediate-release on lipoprotein (a) [Lp(a)], fibrinogen, and certain other independent biochemical risk markers for coronary heart disease are unknown.
The appearance of lovastatin in plasma from an Altoprev® Extended-Release Tablet is slower and more prolonged compared to the lovastatin immediate-release formulation.
A pharmacokinetic study carried out with Altoprev® involved measurement of the systemic concentrations of lovastatin (pro-drug), lovastatin acid (active-drug) and total and active inhibitors of HMG-CoA reductase. The pharmacokinetic parameters in 12 hypercholesterolemic subjects at steady state, after 28 days of treatment, comparing Altoprev® 40 mg to lovastatin immediate-release 40 mg, are summarized in Table 3.
Table 3: Altoprev® vs. Lovastatin Immediate-Release
(IR ) (Steady-State Pharmacokinetic Parameters at Day 28)
|Drug||Cmax (ng/mL)||Cmin (ng/mL)||Tmax (h)||AUC 0-2hr (ng•hr/mL)|
|Altoprev® 40 mg*||5.5||5.8||17.3||13.4||2.6||3.1||9.1||4.3||14.2||11.8||77||87||263||171|
|Lovastatin IR 40 mg**||7.8||11.9||36.2||26.6||0.4||0.7||2.4||2.1||3.3||5.3||45||83||252||186|
|L=lovastatin, LA=lovastatin acid, TI=total inhibitors of
HMG-CoA reductase, AI=active inhibitors of HMG-CoA reductase, Cmax=highest
observed plasma concentration, Cmin=trough concentration at t=24 hours after
dosing, Tmax=time at which the Cmax occurred, AUC0-24hr=area under the plasma
concentration-time curve from time 0 to 24 hr after dosing, calculated by the
linear trapezoidal rule.
* Administered at bedtime.
** Administered with the evening meal.
The mean plasma concentration-time profiles of lovastatin and lovastatin acid in patients after multiple doses of Altoprev® or lovastatin immediate-release at day 28 are shown in Figure 1.
Figure 1 : Mean (SD) plasma concentration-time
profiles of lovastatin and lovastatin acid in hypercholesterolemic patients
(n=12) after 28 days of administration of Altoprev® or lovastatin
The extended-release properties of Altoprev® are characterized by a prolonged absorptive phase, which results in a longer Tmax and lower Cmax for lovastatin (pro-drug) and its major metabolite, lovastatin acid, compared to lovastatin immediate-release.
The bioavailability of lovastatin (pro-drug) as measured by the AUC0-24hr was greater for Altoprev® compared to lovastatin immediate-release (as measured by a chemical assay), while the bioavailability of total and active inhibitors of HMG-CoA reductase were equivalent to lovastatin immediate-release (as measured by an enzymatic assay).
With once-a-day dosing, mean values of AUCs of active and total inhibitors at steady state were about 1.8-1.9 times those following a single dose. Accumulation ratio of lovastatin exposure was 1.5 after multiple daily doses of Altoprev® compared to that of a single dose measured using a chemical assay. Altoprev® appears to have dose linearity for doses from 10 mg up to 60 mg per day.
When Altoprev® was given after a meal, plasma concentrations of lovastatin and lovastatin acid were about 0.5 - 0.6 times those found when Altoprev® was administered in the fasting state, indicating that food decreases the bioavailability of Altoprev®. There was an association between the bioavailability of Altoprev® and dosing after mealtimes. Bioavailability was lowered under the following conditions, (from higher bioavailability to lower bioavailability) in the following order: under overnight fasting conditions, before bedtime, with dinner, and with a high fat breakfast. In a multicenter, randomized, parallel group study, patients were administered 40 mg of Altoprev® at three different times; before breakfast, after dinner and at bedtime. Although there was no statistical difference in the extent of lipid change between the three groups, there was a numerically greater reduction in LDL-C and TG and an increase in HDL-C when Altoprev® was administered at bedtime. Results of this study are displayed in Table 4.
Table 4 : Altoprev® 40 mg (Least Squares Mean Percent
Changes from Baseline to Endpoint at 4 Weeks of Treatment*)
|N=22 for the Before Breakfast group, N=23 for the After
Dinner group, and N=23 for the Before Bedtime group.
*All changes from baseline are statistically significant.
At steady state in humans, the bioavailability of lovastatin, following the administration of Altoprev®, was 190% compared to lovastatin immediate-release.
Absorption of lovastatin, estimated relative to an intravenous reference dose in each of four animal species tested, averaged about 30% of an oral dose. Following an oral dose of 14C-labeled 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. In a single dose study in four hypercholesterolemic patients, it was estimated that less than 5% of an oral dose of lovastatin reaches the general circulation as active inhibitors.
Both lovastatin and its β-hydroxyacid metabolite are highly bound ( > 95%) to human plasma proteins. Animal studies demonstrated that lovastatin crosses the blood-brain and placental barriers.
In animal studies, after oral dosing, lovastatin had high selectivity for the liver, where it achieved substantially higher concentrations than in non-target tissues.
Lovastatin undergoes extensive first-pass extraction in the liver, its primary site of action, with subsequent excretion of drug equivalents in the bile. As a consequence of extensive hepatic extraction of lovastatin, the availability of drug to the general circulation is low and variable.
Metabolism studies with Altoprev® have not been conducted.
Lovastatin is a lactone that is readily hydrolyzed in vivo to the corresponding β-hydroxyacid, a strong inhibitor of HMG-CoA reductase. Inhibition of HMG-CoA reductase is the basis for an assay in pharmacokinetic studies of the β-hydroxyacid metabolites (active inhibitors) and, following base hydrolysis, active plus latent inhibitors (total inhibitors) in plasma following administration of lovastatin.
The major active metabolites present in human plasma are the β-hydroxyacid of lovastatin, its 6'-hydroxy derivative, and two additional metabolites. The risk of myopathy is increased by high levels of HMG-CoA reductase inhibitory activity in plasma. Strong inhibitors of CYP3A can raise the plasma levels of HMG-CoA reductase inhibitory activity and increase the risk of myopathy [see WARNINGS AND PRECAUTIONS, DRUG INTERACTIONS].
Lovastatin is a substrate for CYP3A4 [see DRUG INTERACTIONS]. Grapefruit juice contains one or more components that inhibit CYP3A and can increase the plasma concentrations of drugs metabolized by CYP3A4. In one study1, 10 subjects consumed 200 mL of double-strength grapefruit juice (one can of frozen concentrate diluted with one rather than 3 cans of water) three times daily for 2 days and an additional 200 mL double-strength grapefruit juice together with and 30 and 90 minutes following a single dose of 80 mg lovastatin on the third day. This regimen of grapefruit juice resulted in mean increases in the concentration of lovastatin and its betahydroxyacid metabolite (as measured by the area under the concentration-time curve) of 15-fold and 5-fold respectively (as measured using a chemical assay – liquid chromatography/tandem mass spectrometry). In a second study, 15 subjects consumed one 8 oz glass of single-strength grapefruit juice (one can of frozen concentrate diluted with 3 cans of water) with breakfast for 3 consecutive days and a single dose of 40 mg lovastatin in the evening of the third day. This regimen of grapefruit juice resulted in a mean increase in the plasma concentration (as measured by the area under the concentration-time curve) of active and total HMG-CoA reductase inhibitory activity [using a validated enzyme inhibition assay different from that used in the first study, both before (for active inhibitors) and after (for total inhibitors) base hydrolysis] of 1.34-fold and 1.36-fold, respectively, and of lovastatin and its βhydroxyacid metabolite (measured using a chemical assay – liquid chromatography/tandem mass spectrometry) of 1.94-fold and 1.57fold, respectively. The effect of amounts of grapefruit juice between those used in these two studies on lovastatin pharmacokinetics has not been studied.
TABLE 5 : The Effect of Other Drugs on Lovastatin
Exposure When Both Were Co-administered
|Number of Subjects||Dosing of Coadministered Drug or Grapefruit Juice||Dosing of Lovastatin||AUC Ratio* (with / without coadministered drug) No Effect = 1.00|
|Gemfibrozil||11||600 mg BID for 3 days||40 mg||0.96||2.8|
|Itraconazole‡||12||200 mg QD for 4 days||40 mg on Day 4||> 36§||22|
|10||100 mg QD for 4 days||40 mg on Day 4||> 14.8§||15.4|
|Grapefruit Juice¶ (high dose)||10||200 mL of double-strength TID#||80 mg single dose||15.3||5|
|Grapefruit Juice¶ (low dose)||16||8 oz (about 250 mL) of single-strengthÞ for 4 days||40 mg single dose||1.94||1.57|
|Cyclosporine||16||Not describedβ||10 mg QD for 10 days||5- to 8-fold||NDà|
|Number of Subjects||Dosing of Coadministered Drug or Grapefruit Juice||Dosing of Lovastatin||AUC Ratio* (with / without coadministered drug) No Effect = 1.00|
|Total Lovastatin acidè|
|Diltiazem||10||120 mg BID for 14 days||20 mg||3.57è|
|* Results based on a chemical assay.
† Lovastatin acid refers to the β-hydroxyacid of lovastatin.
‡ The mean total AUC of lovastatin without itraconazole phase could not be determined accurately. Results could be representative of strong CYP3A inhibitors such as ketoconazole, posaconazole, clarithromycin, telithromycin, HIV protease inhibitors, and nefazodone.
§ Estimated minimum change.
¶ The effect of amounts of grapefruit juice between those used in these two studies on lovastatin pharmacokinetics has not been studied.
# Double-strength: one can of frozen concentrate diluted with one can of water. Grapefruit juice was administered TID for 2 days, and 200 mL together with single dose lovastatin and 30 and 90 minutes following single dose lovastatin on Day 3.
Þ Single-strength: one can of frozen concentrate diluted with 3 cans of water. Grapefruit juice was administered with breakfast for 3 days, and lovastatin was administered in the evening on Day 3.
βCyclosporine-treated patients with psoriasis or post kidney or heart transplant patients with stable graft function, transplanted at least 9 months prior to study.
àND = Analyte not determined.
è Lactone converted to acid by hydrolysis prior to analysis. Figure represents total unmetabolized acid and lactone.
In a single-dose study with Altoprev®, the amounts of lovastatin and lovastatin acid excreted in the urine were below the lower limit of quantitation of the assay (1.0 ng/mL), indicating that negligible excretion of Altoprev® occurs through the kidney.
Lovastatin undergoes extensive first-pass extraction in the liver, its primary site of action, with subsequent excretion of drug equivalents in the bile.
Geriatric: Lovastatin Immediate-Release
In a study with lovastatin mmediate-elease which included 16 elderly patients between 70-78 years of age who received lovastatin immediate-release 80 mg/day, the mean plasma level of HMG-CoA reductase inhibitory activity was increased approximately 45% compared with 18 patients between 18-30 years of age [see Use In Specific Populations].
Pediatric: Pharmacokinetic data in the pediatric population are not available.
Gender: In a single dose pharmacokinetic study with Altoprev®, there were no statistically significant differences in pharmacokinetic parameters between men (n=12) and women (n=10), although exposure tended to be higher in men than women.
In clinical studies with Altoprev®, there was no clinically significant difference in LDL-C reduction between men and women.
Renal Impairment: In a study of patients with severe renal impairment (creatinine clearance 10-30 mL/min), the plasma concentrations of total inhibitors after a single dose of lovastatin were approximately two-fold higher than those in healthy volunteers.
Hemodialysis: The effect of hemodialysis on plasma levels of lovastatin and its metabolites have not been studied.
Hepatic Impairment: No pharmacokinetic studies with Altoprev® have been conducted in patients with hepatic impairment.
Altoprev® has been shown to reduce Total-C, LDL-C, and TG and increase HDL-C in patients with hypercholesterolemia. Near maximal response was observed after four weeks of treatment and the response was maintained with continuation of therapy for up to 6 months.
In a 12-week, multicenter, placebo-controlled, double-blind, dose-response study in adult men and women 21 to 70 years of age with primary hypercholesterolemia, once daily administration of Altoprev® 10 to 60 mg in the evening was compared to placebo. Altoprev® produced dose related reductions in LDL-C and Total-C. Altoprev® produced mean reductions in TG across all doses that varied from approximately 10% to 25%. Altoprev® produced mean increases in HDL-C across all doses that varied from approximately 9% to 13%.
The lipid changes with Altoprev® treatment in this study, from baseline to endpoint, are displayed in Table 6.
Table 6 : Altoprev® vs. Placebo (Mean Percent Change
from Baseline After 12 Weeks)*
|Altoprev® 10 mg||33||-23.8||9.4||-17.9||-17.3|
|Altoprev® 20 mg||34**||-29.6||12||-20.9||-13|
|Altoprev® 40 mg||33||-35.8||13.1||-25.4||-9.9|
|Altoprev® 60 mg||35||-40.8||11.6||-29.2||-25.1|
|N= the number of patients with values at both baseline
*Except for the HDL-C elevation with Altoprev® 10 mg, all lipid changes with Altoprev® were statistically significant compared to placebo.
**For LDL-C, 33 patients had values at baseline and endpoint.
The range of LDL-C responses is represented graphically in the following figure (Figure 2):
Figure 2 : Altoprev® vs. Placebo LDL-C Percent Change
from Baseline After 12 Weeks
The distribution of LDL-C responses is represented graphically by the boxplots in Figure 2. The bottom line of the box represents the 25th percentile and the top line, the 75th percentile. The horizontal line in the box represents the median and the gray area is the 95% confidence interval for the median. The range of responses is depicted by the tails and outliers.
Expanded Clinical Evaluation of Lovastatin (EXCEL) Study
Lovastatin Immediate-Release was compared to placebo in 8,245 patients with hypercholesterolemia [Total-C 240-300mg/dL (6.2 mmol/L-7.6 mmol/L), LDL-C > 160 mg/dL (4.1 mmol/L)] in the randomized, double-blind, parallel, 48-week EXCEL study. All changes in the lipid measurements (see Table 7) observed in lovastatin immediate-release-treated patients were dose-related and significantly different from placebo (p ≤ 0.001). These results were sustained throughout the study.
Table 7 : Lovastatin Immediate-Release (IR) vs.
Placebo (Percent Change from Baseline - Average Values Between Weeks 12 and 48)
|DOSAGE||N**||TOTAL-C (mean)||LDL-C (mean)||HDL-C (mean)||LDL-C/ HDL-C (mean)||TOTAL-C/ HDL-C (mean)||TG (median)|
|Lovastatin IR 20 mg q.p.m.||1642||-17||-24||6.6||-27||-21||-10|
|40 mg q.p.m.||1645||-22||-30||7.2||-34||-26||-14|
|20 mg b.i.d.||1646||-24||-34||8.6||-38||-29||-16|
|40 mg b.i.d.||1649||-29||-40||9.5||-44||-34||-19|
Altoprev® Long-Term Study
A total of 365 patients were enrolled in an extension study in which all patients were administered Altoprev® 40 mg or 60 mg once daily for up to 6 months of treatment. The lipid-altering effects of Altoprev® were comparable to what was observed in the dose-response study, and were maintained for up to 6 months of treatment.
In clinical studies with Altoprev®, there were no statistically significant differences in LDL-C reduction in an older population ( ≥ 65 years old), compared to a younger population ( < 65 years old). There were also no statistically significant differences in LDL-C reduction between male and female patients.
Heterozygous Familial Hypercholesterolemia
Lovastatin Immediate-Release has been shown to be effective in reducing Total-C and LDL-C in heterozygous familial and non-familial forms of primary hypercholesterolemia and in mixed hyperlipidemia. A marked response was seen within 2 weeks, and the maximum therapeutic response occurred within 4-6 weeks. The response was maintained during continuation of therapy. Single daily doses given in the evening were more effective than the same dose given in the morning, perhaps because cholesterol is synthesized mainly at night.
Lovastatin immediate-Release was studied in controlled trials in hypercholesterolemic patients with well-controlled non-insulin dependent diabetes mellitus with normal renal function. The effect of lovastatin immediate-release on lipids and lipoproteins and the safety profile of lovastatin immediate-release were similar to that demonstrated in studies in nondiabetics. Lovastatin Immediate-Release had no clinically important effect on glycemic control or on the dose requirement of oral hypoglycemic agents.
Prevention of Coronary Heart Disease
The Air Force/Texas Coronary Atherosclerosis Prevention Study (AFCAPS/TexCAPS), a double-blind, randomized, placebo-controlled, primary prevention study, demonstrated that treatment with lovastatin immediate-release decreased the rate of acute major coronary events (composite endpoint of myocardial infarction, unstable angina, and sudden cardiac death) compared with placebo during a median of 5.1 years of follow-up. Participants were middle-aged and elderly men (ages 45-73) and women (ages 55-73) without symptomatic cardiovascular disease with average to moderately elevated Total-C and LDL-C, below average HDL-C, and who were at high risk based on elevated Total-C/HDL-C. In addition to age, 63% of the participants had at least one other risk factor (baseline HDL-C < 35 mg/dL, hypertension, family history, smoking and diabetes).
AFCAPS/TexCAPS enrolled 6,605 participants (5,608 men, 997 women) based on the following lipid entry criteria: Total-C range of 180-264 mg/dL, LDL-C range of 130-190 mg/dL, HDL-C of ≤ 45 mg/dL for men and ≤ 47 mg/dL for women, and TG of ≤ 400 mg/dL. Participants were treated with standard care, including diet, and either lovastatin immediate-release 20 mg - 40 mg daily (n= 3,304) or placebo (n= 3,301). Approximately 50% of the participants treated with lovastatin immediate-release were titrated to 40 mg daily when their LDL-C remained > 110 mg/dL at the 20-mg starting dose.
Lovastatin Immediate-Release reduced the risk of a first acute major coronary event, the primary efficacy endpoint, by 37% (lovastatin immediate-release 3.5%, placebo 5.5%; p < 0.001; Figure 3). A first acute major coronary event was defined as myocardial infarction (54 participants on lovastatin immediate-release, 94 on placebo) or unstable angina (54 vs. 80) or sudden cardiac death (8 vs. 9). Furthermore, among the secondary endpoints, lovastatin immediate-release reduced the risk of unstable angina by 32% (1.8% vs. 2.6%; p=0.023), of myocardial infarction by 40% (1.7% vs. 2.9%; p=0.002), and of undergoing coronary revascularization procedures (e.g., coronary artery bypass grafting or percutaneous transluminal coronary angioplasty) by 33% (3.2% vs. 4.8%; p=0.001). Trends in risk reduction associated with treatment with lovastatin immediate-release were consistent across men and women, smokers and nonsmokers, hypertensives and non-hypertensives, and older and younger participants. Participants with ≥ 2 risk factors had risk reductions (RR) in both acute major coronary events (RR 43%) and coronary revascularization procedures (RR 37%). Because there were too few events among those participants with age as their only risk factor in this study, the effect of lovastatin immediate-release on outcomes could not be adequately assessed in this subgroup.
Figure 3 : Acute Major Coronary Events (Primary
In the Canadian Coronary Atherosclerosis Intervention Trial (CCAIT), the effect of therapy with lovastatin on coronary atherosclerosis was assessed by coronary angiography in hyperlipidemic patients. In this randomized, double-blind, controlled clinical trial, patients were treated with conventional measures (usually diet and 325 mg of aspirin every other day) and either lovastatin 20 mg - 80 mg daily or placebo. Angiograms were evaluated at baseline and at two years by computerized quantitative coronary angiography (QCA). Lovastatin significantly slowed the progression of lesions as measured by the mean change per-patient in minimum lumen diameter (the primary endpoint) and percent diameter stenosis, and decreased the proportions of patients categorized with disease progression (33% vs. 50%) and with new lesions (16% vs. 32%).
In a similarly designed trial, the Monitored Atherosclerosis Regression Study (MARS), patients were treated with diet and either lovastatin 80 mg daily or placebo. No statistically significant difference between lovastatin and placebo was seen for the primary endpoint (mean change per patient in percent diameter stenosis of all lesions), or for most secondary QCA endpoints. Visual assessment by angiographers who formed a consensus opinion of overall angiographic change (Global Change Score) was also a secondary endpoint. By this endpoint, significant slowing of disease was seen, with regression in 23% of patients treated with lovastatin compared to 11% of placebo patients.
The effect of lovastatin on the progression of atherosclerosis in the coronary arteries has been corroborated by similar findings in another vasculature. In the Asymptomatic Carotid Artery Progression Study (ACAPS), the effect of therapy with lovastatin on carotid atherosclerosis was assessed by B-mode ultrasonography in hyperlipidemic patients with early carotid lesions and without known coronary heart disease at baseline. In this double- blind, controlled clinical trial, 919 patients were randomized in a 2 x 2 factorial design to placebo, lovastatin 10-40 mg daily and/or warfarin. Ultrasonograms of the carotid walls were used to determine the change per patient from baseline to three years in mean maximum intimal-medial thickness (IMT) of 12 measured segments. There was a significant regression of carotid lesions in patients receiving lovastatin alone compared to those receiving placebo alone (p=0.001). The predictive value of changes in IMT for stroke has not yet been established. In the lovastatin group there was a significant reduction in the number of patients with major cardiovascular events relative to the placebo group (5 vs. 14) and a significant reduction in all-cause mortality (1 vs. 8).
There was a high prevalence of baseline lenticular opacities in the patient population included in the early clinical trials with lovastatin immediate-release. During these trials the appearance of new opacities was noted in both the lovastatin immediate-release and placebo groups. There was no clinically significant change in visual acuity in the patients who had new opacities reported nor was any patient, including those with opacities noted at baseline, discontinued from therapy because of a decrease in visual acuity.
A three-year, double-blind, placebo-controlled study in hypercholesterolemic patients to assess the effect of lovastatin immediate-release on the human lens demonstrated that there were no clinically or statistically significant differences between the lovastatin immediate-release and placebo groups in the incidence, type or progression of lenticular opacities. There are no controlled clinical data assessing the lens available for treatment beyond three years.
1. Kantola, T, et al. Clin Pharmacol Ther 1998; 63(4):397-402.
2. Manson, J.M., Freyssinges, C., Ducrocq, M.B., Stephenson, W.P., Postmarketing Surveillance of Lovastatin and Simvastatin Exposure During Pregnancy. Reproductive Toxicology. 19(6):439-446. 1996.
Last reviewed on RxList: 1/25/2013
This monograph has been modified to include the generic and brand name in many instances.
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