Scientific Newsroom

The press releases below are specifically related to scientific and clinical public disclosure made by Esperion.

These are being provided for media professionals who write on scientific topics. For the complete list of all Esperion news please see this page.

CLEAR Programs Media Kit

CLEAR Outcomes Trial: Study Rationale and Design

Although statins play a critical role in preventing atherosclerotic cardiovascular disease by lowering LDL cholesterol (LDL-C), 1 they are not always effective enough to get patients to their recommended targets. 2 About two-thirds of patients in the United States – 8.7 million people — have not reached their LDL-C goals despite statin treatment, 3 increasing their risk of heart attack, stroke, and death. 4
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The CLEAR (Cholesterol Lowering via Bempedoic Acid, an ACL-inhibiting Regimen) Outcomes study is a randomized, double-blind, placebo-controlled clinical trial designed to determine whether bempedoic acid reduces the risk of cardiovascular events including cardiovascular death in people at high risk of these events. 
On Dec. 7, 2022, Esperion announced that CLEAR Outcomes met its primary endpoint, demonstrating a statistically significant risk reduction in MACE-4 in patients treated with 180 mg/day bempedoic acid compared with placebo.  (MACE-4, or major adverse cardiovascular events, is a composite endpoint that includes cardiovascular death, nonfatal MI, nonfatal stroke, and coronary revascularization; see below for details.)
This is an investigational trial. The effects of NEXLETOL on cardiovascular morbidity and mortality have not been determined.
Launched in November 2016, the study enrolled 13,970 patients in 32 countries. Patients were randomized to either 180 mg of bempedoic acid daily or a placebo with an estimated mean follow up duration of 3.5 years. 
Inclusion criteria:
  • Ages 18-85
  • History of cardiovascular disease, including coronary artery disease, symptomatic peripheral arterial disease, cerebrovascular atherosclerotic disease, or at high risk for having a cardiovascular event
  • Patient-reported history of statin intolerance defined as an adverse effect that started or increased during statin therapy and resolved or improved after therapy discontinued.  Intolerance was due to inability to tolerate two or more statins at any dose or 1 statin at any dose and unwilling or advised by a physician to not attempt a second statin.  Both the patient and investigator were required to provide written confirmation that the patient was aware of the benefits of statins to reduce the risk of cardiovascular events, including death, and acknowledge that many other patients who are unable to tolerate a statin can tolerate a different statin or dose.
  • Men and non-pregnant, non-lactating women
  • Fasting blood LDL-C ≥ 100 (2.6 mmol/L) at screening while receiving stable background lipid lowering therapy
Exclusion criteria:
  • Fasting blood triglycerides > 500 mg/dL (5.6 mmol/L) at screening
  • Recent (within 90 days of screening) history of major cardiovascular events, transient ischemic attack, or unstable or symptomatic cardiac arrhythmia
  • History of severe heart failure
  • Uncontrolled hypertension or uncontrolled diabetes
Primary endpoint:
The time to first occurrence of any of the following:
  • Cardiovascular death
  • Nonfatal myocardial infarction 
  • Nonfatal stroke
  • Coronary revascularization 4
Key Secondary Time to Event Endpoints: 
  • Time to first occurrence of the composite endpoint of CV death, nonfatal MI, or nonfatal stroke (MACE-3)
  • Time to first occurrence of (fatal + nonfatal) MI
  • Time to first occurrence of coronary revascularization
  • Time to first occurrence of (fatal + nonfatal) stroke
  • Time to CV death
  • Time to all-cause mortality
Secondary Efficacy Lipid and Biomarker Endpoints:
  • Percent change from baseline to Month 6 in LDL-C
  • Percent change from baseline to Month 6 in hsCRP
  • Absolute change from baseline to Month 12 in HbA1c in patients in the inadequately controlled diabetes efficacy population (patients with type 2 diabetes mellitus and an HbA1c of 7% or greater at baseline)
CLEAR Outcomes was an event-driven clinical trial that continued until all of the following criteria were met: 
At least 1,620 adjudicated primary endpoints were accrued.
At least 810 patients experienced an adjudicated secondary composite endpoint event of cardiovascular death, nonfatal myocardial infarction, or non-fatal stroke.
24 months had elapsed since last patient was randomized
Assuming a 3.59% annual event rate in the placebo group and an estimated lost-to-follow up rate of 1% per year, a total sample size of 14,000 patients provided more than 95% power to detect a 17% reduction in the primary endpoint with bempedoic acid.4
For more details, see the full study design here.

Interesting Note on Patient Population:

  • The proportion of women in CLEAR Outcomes (48.2%) reflects the prevalence of heart disease in U.S. women overall. This is a significant improvement over the historical underrepresentation of women in cardiovascular clinical trials. 5
    • Enrollment of women in other cardiovascular outcomes trials has ranged from 24% 6 to 38% 7 of total enrollment. 
    • The increased representation of women in CLEAR Outcomes is especially important given that women are significantly more likely than men to experience statin intolerance.8

FACTS AND FIGURES: Cholesterol and Atherosclerotic Heart Disease (ASCVD)

ASCVD: Prevalence, causes and consequences
Atherosclerotic cardiovascular disease (ASCVD) is the leading cause of illness and death in the United States and around the world.
  • In the U.S., it affects an estimated 10 percent of the adult population, or about 24 million people. 9 
  • Someone in the United States dies every 34 seconds from cardiovascular disease, accounting for one in every five deaths. 10 
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Despite what we know about the risk factors for developing ASCVD and how to treat it, the death toll continues to rise; the U.S. Centers for Disease Control and Prevention estimates that heart disease-related deaths will increase 25 percent by 2030.  
Men and women have a similar risk of heart disease, but events such as myocardial infarction often cause different symptoms in women, sometimes presenting as indigestion or back pain instead of the more “classic” symptoms such as chest pain. 11 An estimated 805,000 myocardial infarctions occur each year, and 20 percent of those attacks are believed to be “silent,” described as a person not knowing the event is happening, but considerable damage occurs. 10 
Causes and consequences

ASCVD involves the buildup of fatty plaque inside arteries that can create life-threatening scenarios 

  • Plaque buildup narrows the arteries, reducing or preventing blood flow.
  • Plaque can rupture inside arteries, creating dangerous clots that can block blood flow to the heart, brain, or other parts of the body.

ASCVD can lead to serious and sometimes deadly cardiovascular events such as:

  • Myocardial infarction
  • Stroke or transient ischemic attack
  • Angina 
  • Peripheral artery disease

People with ASCVD who have had a first myocardial infarction, stroke, or other event are at increased risk of additional events. Over time, ASCVD can result in heart failure and other chronic, debilitating illness, and results in more than $200 billion USD each year in healthcare services, medicines, and lost productivity. 11

The role of cholesterol in ASCVD

The role of elevated levels of LDL-cholesterol (LDL-C) in ASCVD is acknowledged and well understood. 12 Multiple studies have shown that lowering LDL-C reduces the risk of cardiovascular events among people with ASCVD. To date, research has not demonstrated a low threshold where the risk-reduction benefit stops. 1 As a result, treatment guidelines have focused on LDL-C lowering as a cornerstone in both prevention and management of ASCVD, predominantly through lipid-lowering medicines.

Treating ASCVD: Significant gaps remain 

Statins are proven to be effective in lowering LDL-C and reducing adverse cardiac events, and are considered first-line therapy for lowering LDL-C. When they were first introduced, “getting to goal” became the mantra among both physicians and patients with high LDL cholesterol. 

Yet nearly 30 years later, about two-thirds of people with ASCVD in the U.S. still are not at their LDL-C goal, despite the availability of statin treatment. 13 This leads to many repeat strokes, myocardial infarctions, revascularization procedures, and deaths that might have been prevented.  

For very high-risk patients (those with existing ASCVD):

  • The American Heart Association (AHA)/American College of Cardiology (ACC) Task Force on Clinical Practice Guidelines recommends a target LDL-C of <70 mg/dL. 12
  • European Society of Cardiology (ESC)/European Atherosclerosis Society (EAS) Guidelines for the Management of Dyslipidemias suggest a lower target LDL-C of < 55 mg/dL. 14 

Yet a 2019 analysis of medical records of ASCVD patients in U.S. commercial and Medicare health plans found that the majority of patients did not achieve the AHA/ACC guideline-recommended LDL-C goal of <70 mg/dL. In fact, more than one-third (37.5 percent) had LDL-C levels of 100 mg/dL or higher. 13

  • Specifically, 56.2% of these patients experienced a recent acute coronary syndrome, 69.2% of patients had an ischemic stroke, 80.8% of patients had a diagnosis of PAD, and 71.5% of patients had a diagnosis of coronary artery disease. 13 
Still not getting to goal: Contributing to the treatment gap

Despite widespread statin use, discontinuation and/or lack of adherence to statin treatment continues to be a major gap in both preventing and treating ASCVD: 15

  • A key compliance barrier is limitations from side effects, notably myopathies. 16 
  • One-third of people taking statins stop treatment within a year. 17
  • Women and people of Asian ethnicity are at particular risk of statin-related side effects. 18
Non-statin treatment options

Patients not achieving LDL-C targets on statins alone may benefit from combination therapy. There are a number of proven options for patients and physicians to consider:  

  • PCSK9 inhibitors can lower LDL-C substantially (by more than 50% in people with very high baseline LDL-C levels) with no increase in muscle-related side effects among people with statin intolerance, 19 but they must be injected and cost significantly more than other treatments, both of which are barriers to widespread use. 4
  • Bempedoic acid has been shown to significantly reduce LDL-C and is approved for use in combination with diet and maximally tolerated statin therapy for adults with established ASCVD who require additional LDL-C lowering to reach their treatment goals. 20 Bempodoic acid is also available in a fixed dose combination with ezetimibe. The effects of NEXLETOL and NEXLIZET on cardiovascular morbidity and mortality have not been determined.
  • The cholesterol absorption inhibitor ezetimibe can lower LDL-C levels 18% to 20%, with minimal rates of muscle-related side effects. 21 But treatment with ezetimibe alone is often unsuccessful at getting people to their LDL-C treatment goals. 4
  • Ezetimibe inhibition of cholesterol absorption from the small intestine provides a complementary LDL-C-lowering mechanism of action to bempedoic acid; these two agents are offered as a fixed-combination drug product (FCDP) under the brand name Nexlizet.® Nexlizet has been proven to lower LDL cholesterol an additional 38% relative to placebo when added to maximally tolerated statin therapy. 22


Bempedoic Acid: Mechanism of Action & Scientific Development
Bempedoic acid (BA) represents a new class of drug that lowers LDL-cholesterol (LDL-C) through a unique mechanism of action, making it an important treatment option for people at high risk of atherosclerotic cardiac events who cannot tolerate statins – or for whom statins are not enough to help them achieve their target LDL-C goals. 
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Bempedoic acid acts by inhibiting the enzyme ATP-citrate lyase (ACL), which plays a critical role in lipid metabolism and is found at the nexus of the cholesterol and triglyceride biosynthesis pathways, before these two pathways diverge. BA works two steps upstream from HMG-CoA reductase (the site of action for statins). 23
A prodrug, bempedoic acid is primarily activated in the liver, where it inhibits ACL. Unlike statins, it is not activated in skeletal muscle,22 23 24 25 offering the potential to avoid the muscle pain and weakness (myopathy) statins can cause. Bempedoic acid’s inhibition of ACL increases levels of LDL receptors in the liver, which adhere to circulating LDL particles, reducing LDL-C levels in the blood.22 
Because BA’s mechanism of action is different from other lipid-lowering therapies, it can be combined with other treatments to further lower LDL-C. This makes it an important treatment option in patients for whom statins alone are not effective in achieving their LDL-C goal or for those who experience side effects with statin therapy.
Importantly, bempedoic acid’s safety profile is generally comparable to placebo.
Click here for a video that describes bempedoic acid’s mechanism of action in more detail.
Scientific Development of Bempedoic Acid
Five randomized, double-blind, placebo-controlled, parallel-group, phase 3 multicenter clinical trials known as Cholesterol Lowering via Bempedoic Acid, an ACL-inhibiting Regimen (CLEAR) have established the safety, tolerability, and efficacy of bempedoic acid in lowering LDL-C in a total of 3,623 participants.  
CLEAR Clinical Trials: Phase 3/4
StudyPublicationKey Results
CLEAR TranquilityBallantyne et al. Atherosclerosis. 2018;277:195-203BA added to background lipid-modifying therapy that included ezetimibe reduced LDL-C by 28.5% (placebo-corrected) from baseline (95% CI; p < 0.001).
CLEAR HarmonyRay et al. N Engl J Med. 2019 ;380: 1022-1032BA added to background lipid-modifying therapy reduced mean LDL-C by 18.1% (placebo corrected) from baseline (95% CI; p<0.001).
CLEAR SerenityLaufs et al. J Am Heart Assoc. 2019;8 :e011662BA added to background lipid-modifying therapy reduced LDL-C by 21.4% (placebo-corrected) from baseline (95% CI; p<0.001)
CLEAR WisdomGoldberg et al. JAMA. 2019;322: 1780-1788BA added to background lipid-modifying therapy reduced LDL-C by 17.4% (placebo-corrected) from baseline (95% CI, p <0.001).
BA + ezetimibe fixed-dose combination (FDC) Ballantyne et al. Eur J Prev Cardiol.
2020; 27(6): 593–603

BA + ezetimibe FDC added to background lipid-modifying therapy reduced LDL-C significantly more than placebo (-38%, placebo-corrected), ezetimibe alone (-23.2%) or BA alone (-7.2%); p < 0.001.
CLEAR OutcomesNot yet published.Met primary endpoint, demonstrating statistically significant risk reduction in MACE-4 in patients treated with 180 mg/day bempedoic acid compared with placebo. This is an investigational trial. The effects of NEXLETOL on cardiovascular morbidity and mortality have not been determined.

LDL-C-Lowering Properties of Bempedoic Acid: Additional Studies of Interest

Ballantyne C et al. Factors Associated With Enhanced Low-Density Lipoprotein Cholesterol Lowering With Bempedoic Acid. J Am Heart Assoc. 2022;11(15): e024531. 
This post-hoc analysis used pooled data from four phase 3 studies of bempedoic acid (BA) compared with placebo to determine what factors may contribute to the highest LDL-C reductions (30% or more) seen in these studies. The analysis identified the following factors (p<0.01 for each): 
  • Not taking statins
  • Being female
  • Having a history of diabetes
  • Concurrent use of the lipid-lowering therapy ezetimibe
  • An increased level of high-sensitivity C-reactive protein at baselin
Read More
“A large percentage of patients receiving BA achieved LDL-C reductions comparable to a moderate- or high-intensity statin,” the authors wrote, concluding that the above factors “may be useful to identify patients who may have a greater LDL-C reduction with BA.” 
Gunn L et al. Estimated cardiovascular benefits of bempedoic acid in patients with established cardiovascular disease. Atherosclerosis Plus. 2022;49: 20-27.
This study assessed the potential cardiovascular benefits of bempedoic acid through a simulation study in patients with atherosclerotic cardiovascular disease (ASCVD) and elevated LDL-C.
Researchers used the validated SMART prediction model to predict the baseline 10-year risk of cardiovascular death, non-fatal heart attack, and non-fatal stroke) in people with ASCVD who were enrolled in four Phase 3, randomized, placebo-controlled studies of bempedoic acid. (The SMART model incorporates factors such as age, sex, smoking status, systolic blood pressure, history of diabetes, history of coronary artery disease, and levels of HDL-C. 
They analyzed two groups of patients: those who were taking moderate to high doses of statins, and those who could only tolerate a low-dose statin (most patients in this group were not taking statins). The analysis predicted a reduced risk of cardiovascular events over time in both groups, with a more significant predicted benefit among patients with statin intolerance.
In the statin group, “if this reduction in LDL-C was maintained with continued treatment over 10 years, the predicted impact with bempedoic acid on the 10-year cardiovascular risk would translate to a 10.6% risk reduction relative to baseline, and an absolute difference of 3.3% compared with the placebo group,” the authors concluded.
In the statin-intolerant group, “if maintained over 10 years with treatment, the reduction in LDL-C with bempedoic acid therapy would be expected to result in a 18.9% relative reduction in cardiovascular risk,” the authors predicted. “Thus, the predicted 10-year cardiovascular risk with bempedoic acid would be estimated to be 6.0% lower with bempedoic acid than with placebo.”

Important Safety Information

NEXLETOL and NEXLIZET are indicated as adjuncts to diet and maximally tolerated statin therapy for the treatment of adults with heterozygous familial hypercholesterolemia or established atherosclerotic cardiovascular disease who require additional lowering of LDL-C.
Limitations of Use: The effect of NEXLETOL and NEXLIZET on cardiovascular morbidity and mortality has not been determined.
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Contraindications: NEXLETOL has no contraindications. NEXLIZET is contraindicated in patients with a known hypersensitivity to ezetimibe tablets. Hypersensitivity reactions including anaphylaxis, angioedema, rash, and urticaria have been reported with ezetimibe.

Warnings and Precautions: Hyperuricemia: Bempedoic acid, a component of NEXLETOL and NEXLIZET, may increase blood uric acid levels. Hyperuricemia may occur early in treatment and persist throughout treatment, and may lead to the development of gout, especially in patients with a history of gout. Assess uric acid levels periodically as clinically indicated. Monitor for signs and symptoms of hyperuricemia, and initiate treatment with urate-lowering drugs as appropriate.

Tendon Rupture: Bempedoic acid is associated with an increased risk of tendon rupture or injury. In clinical trials, tendon rupture occurred in 0.5% of patients treated with bempedoic acid versus 0% of patients treated with placebo, and involved the rotator cuff (the shoulder), biceps tendon, or Achilles tendon. Tendon rupture occurred within weeks to months of starting bempedoic acid. Tendon rupture may occur more frequently in patients over 60 years of age, patients taking corticosteroid or fluoroquinolone drugs, patients with renal failure, and patients with previous tendon disorders. Discontinue NEXLETOL or NEXLIZET at the first sign of tendon rupture. Avoid NEXLETOL and NEXLIZET in patients who have a history of tendon disorders or tendon rupture.

Adverse Reactions: In NEXLETOL clinical trials, the most commonly reported adverse reactions were upper respiratory tract infection, muscle spasms, hyperuricemia, back pain, abdominal pain or discomfort, bronchitis, pain in extremity, anemia, and elevated liver enzymes. Reactions reported less frequently, but still more often than with placebo, included benign prostatic hyperplasia and atrial fibrillation.

In the NEXLIZET clinical trial, the most commonly reported adverse reactions observed with NEXLIZET, but not observed in clinical trials of bempedoic acid or ezetimibe, a component of NEXLIZET, and occurring more frequently than with placebo, were urinary tract infection, nasopharyngitis, and constipation.

Adverse reactions reported in clinical trials of ezetimibe, and occurring at an incidence greater than with placebo, included upper respiratory tract infection, diarrhea, arthralgia, sinusitis, pain in extremity, fatigue, and influenza. Other adverse reactions reported in postmarketing use of ezetimibe included hypersensitivity reactions, including anaphylaxis, angioedema, rash, and urticaria; erythema multiforme; myalgia; elevated creatine phosphokinase; myopathy/rhabdomyolysis; elevations in liver transaminases; hepatitis; abdominal pain; thrombocytopenia; pancreatitis; nausea; dizziness; paresthesia; depression; headache; cholelithiasis; cholecystitis.

Drug Interactions: Simvastatin and Pravastatin: Concomitant use with bempedoic acid results in increased concentrations and increased risk of simvastatin or pravastatin-related myopathy. Use of either NEXLETOL or NEXLIZET with greater than 20 mg of simvastatin or 40 mg of pravastatin should be avoided.

Cyclosporine: Caution should be exercised when using NEXLIZET and cyclosporine concomitantly due to increased exposure to both ezetimibe and cyclosporine. Monitor cyclosporine concentrations in patients receiving NEXLIZET and cyclosporine. In patients treated with cyclosporine, the potential effects of the increased exposure to ezetimibe from concomitant use should be carefully weighed against the benefits of alterations in lipid levels provided by NEXLIZET.

Fibrates: Coadministration of NEXLIZET with fibrates other than fenofibrate is not recommended. Fenofibrate and ezetimibe may increase cholesterol excretion into the bile, leading to cholelithiasis. If cholelithiasis is suspected in a patient receiving NEXLIZET and fenofibrate, gallbladder studies are indicated and alternative lipid-lowering therapy should be considered.

Cholestyramine: Concomitant use of NEXLIZET and cholestyramine decreases ezetimibe concentration. This may result in a reduction of efficacy. Administer NEXLIZET either at least 2 hours before, or at least 4 hours after, bile acid sequestrants.

Lactation and Pregnancy: It is not recommended that NEXLETOL or NEXLIZET be taken during breastfeeding. Discontinue NEXLETOL or NEXLIZET when pregnancy is recognized, unless the benefits of therapy outweigh the potential risks to the fetus. Based on the mechanism of action of bempedoic acid, NEXLETOL and NEXLIZET may cause fetal harm.

Please see full Prescribing Information here.


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