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atorvastatin + ezetimibe (CKD 391 / CKD391)

✓ Approved

Chong Kun Dang Pharmaceutical · HMGCR · Small Molecule

What is atorvastatin + ezetimibe?

atorvastatin + ezetimibe is a small molecule developed by Chong Kun Dang Pharmaceutical. It is approved for therapeutic indications via oral (po).

Drug Profile

Brand NamesCKD 391, CKD391
CompanyChong Kun Dang Pharmaceutical
Drug ClassSmall Molecule
Molecular TargetHMGCR, NPC1L1
RouteOral (PO)
StatusApproved
Sources: ClinicalTrials.gov, Chong Kun Dang Pharmaceutical

Mechanism of Action

Molecular Targets

atorvastatin + ezetimibe acts on 2 molecular targets:

HMGCR3-hydroxy-3-methylglutaryl-CoA reductase (LDLCQ3, LGMDR28)
NPC1L1NPC1 like intracellular cholesterol transporter 1 (SLC65A2, LDLCQ7)
Want deeper analysis?Noah AI can explain complex mechanisms and compare to similar drugs.

Therapeutic Indications

atorvastatin + ezetimibe is developed for 2 unique indications across 1 therapeutic area.

Therapeutic AreaConditionPhase
Metabolism and nutrition disordersHypercholesterolaemia✓ Approved
Metabolism and nutrition disordersHyperlipidaemia✓ Approved

Related Research Articles

PubMedJournal of clinical medicine2026-10-16

Ezetimibe Versus Alirocumab and Plaque Vulnerability in Patients with Acute Coronary Syndrome Not Achieving LDL-Cholesterol Target with Statin Therapy: The COMBI-LLT-ACS Randomized Trial.

Kovalskaya Anna A, Bikbaeva Guzel G, Duplyakov Dmitry D, Duplyakova Polina P et al.

Objective: To compare two lipid-lowering therapy strategies involving Ezetimibe and Alirocumab on the vulnerability of atherosclerotic plaque (AP) in patients with acute coronary syndrome (ACS) not achieving the LDL-cholesterol target while on intensive statin therapy. Methods: Combi-LLT-ACS (Patients receiving combination lipid-lowering therapy admitted with the acute coronary syndrome) included 125 patients aged 59 (51; 64) years, of whom 67.2% were men. All underwent percutaneous coronary intervention of the IRA; also, all patients had at least one stenosis < 50% in non-IRA, had high compliance with statins, and did not reached LDL-C level of ≤1.4 mmol/L. Patients underwent Coronary Computed Tomography Angiography (CCTA) to detect vulnerable AP as well as lipid profile and numerous biomarkers: neutrophil to lymphocyte ratio (NLR), monocyte to lymphocyte ratio (MLR), monocyte to high-density lipoprotein ratio (MHR), systemic inflammatory response index (SIRI), matrix metalloprotease type 9 (MMP-9), tissue inhibitor of metalloproteinases type 1 (TIMP-1), Galectin-3 (GAL-3), neutrophil gelatinase-associated lipocalin (NGAL), and C-reactive protein (CRP). Thereafter, they were randomized into two groups, Ezetimibe vs. Alirocumab, on the same visit. The follow-up period was 52 weeks. We used the following CCTA criteria to detect vulnerable AP: positive remodeling, napkin-ring sign, spotty calcification, and low-attenuation plaque. Results: One month after ACS, vulnerable APs were observed by CCTA in 56 patients (44.8%). After 52 weeks, 10 (17.9%) patients showed stabilization of previously vulnerable APs or a decrease in the number of AP vulnerability criteria. At week 52, TC and LDL-C levels decreased significantly over time in both groups. Both arms of therapy demonstrated a positive effect on the inflammatory markers and markers of extracellular matrix remodeling. Direct comparison of changes between groups revealed no statistically significant differences in the number of vulnerability criteria (p = 0.930); however, in the group receiving Ezetimibe, we found a statistically significant change over the observation period (p = 0.032). Conclusions: Among patients with ACS, receiving a high-intensity statin in combination with Ezetimibe or Alirocumab prevented the emergence of new vulnerable coronary lesions over 52 weeks. While direct regression of specific vulnerability criteria was not observed, these therapeutic strategies were associated with a reduction in LDL-C and biomarkers of inflammation and extracellular matrix remodeling.

PMID 42882025
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PubMedJournal of the American Heart Association2026-10-16

Association of Non-Cytochrome P450 3A4-Metabolized Statins Versus Atorvastatin With Major Adverse Cardiovascular Events in Patients With Cancer Receiving Tyrosine Kinase Inhibitors: A Propensity Score-Matched Target Trial Emulation.

Liao Jing-Huan JH, Chang Wei-Cheng WC, Jhou Hong-Jie HJ, Chen Hsin-Yu HY et al.

Tyrosine kinase inhibitors (TKIs) often undergo CYP3A4 (cytochrome P450 3A4) metabolism. Atorvastatin is a CYP3A4 substrate, whereas rosuvastatin and pitavastatin largely bypass this pathway. We evaluated whether statin choice was associated with major adverse cardiovascular events in TKI-treated patients with cancer. Using TriNetX, we conducted an active-comparator, new-user target trial emulation among adults with cancer receiving their first TKI. The index date was the first statin dispensation; outcome ascertainment began on Day 30 and continued up to 3 years. Separate 1:1 propensity score-matched comparisons included rosuvastatin versus atorvastatin (primary; 2215 per group), pitavastatin comparisons, and a pooled non-CYP3A4 statin comparison. Among 10 843 eligible patients (mean age, 66.7 years; 60.7% male), rosuvastatin was associated with a lower major adverse cardiovascular events rate than atorvastatin (624 versus 769 events; hazard ratio [HR], 0.84 [95% CI, 0.76-0.93]). The proportional-hazards assumption was violated (P=0.042), so the HR was interpreted as a time-averaged association. The pooled comparison was concordant (HR, 0.87 [95% CI, 0.78-0.96]). The early-persistence Day-180 estimate was imprecise (HR, 0.90 [95% CI, 0.73-1.09]). Rosuvastatin use was associated with lower major adverse cardiovascular events than atorvastatin in TKI-treated patients with cancer. This observational finding is compatible with, but does not establish, a CYP3A4-mediated interaction. Residual confounding, nonaligned TKI and statin timing in part of the primary cohort, and lack of individual-level event-time data require prospective confirmation.

PMID 42885792
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PubMedMolecules (Basel, Switzerland)2026-10-16

Distinct Inhibitory Effects of Statin Lactones on Ca2+- and Na+/K+-ATPases.

Cruz-Cortés Carlos C, Šeflová Jaroslava J, Espinoza-Fonseca L Michel LM

P-type ATPases share a conserved catalytic architecture but have different sensitivities to small-molecule inhibitors. We previously identified several statins as inhibitors of the sarco/endoplasmic reticulum Ca2+-ATPase (SERCA), but the extent to which this inhibitory activity reflects broader pharmacological cross-reactivity among P-type ATPases remains unknown. Here, we compared the effects of seven structurally diverse statin lactones, which share a common δ-lactone moiety but contain distinct core scaffolds, including hexahydronaphthalene-based and aromatic heterocyclic ring systems, on SERCA and the Na+/K+-ATPase (NKA). The structurally related lovastatin and simvastatin produced similar concentration-dependent inhibitory profiles toward SERCA and NKA, despite the otherwise distinct pharmacological sensitivities of these pumps. In contrast, atorvastatin, rosuvastatin, and pitavastatin showed more divergent inhibitory profiles, generally with greater inhibition of SERCA than NKA at higher concentrations. Pravastatin and fluvastatin, however, had minimal effects on either ATPase over the concentration range examined. These findings build on our previous identification of selected statins as SERCA inhibitors by demonstrating that their activity can extend to NKA. Overall, the results reveal substantial structure-dependent variation in the effects of statin lactones on these P-type ATPases, ranging from convergent inhibition to differential inhibition and minimal activity.

PMID 42883189
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PubMedAtherosclerosis plus2026-10-15

Lipoprotein(a) and early LDL-cholesterol target attainment after a first acute coronary syndrome: a real-world cohort study.

Riera-Molist Núria N, Puigoriol Juvanteny Emma E, Swedzky Federico F, Goutan-Roura Ester E et al.

Despite intensive lipid-lowering therapy, early attainment of the guideline-recommended LDL-cholesterol (LDL-C) target after acute coronary syndrome (ACS) remains suboptimal. Baseline factors associated with early LDL-C target attainment remain incompletely characterized, particularly the role of lipoprotein(a) [Lp(a)]. We aimed to assess early LDL-C target attainment after a first ACS and identify baseline factors associated with target attainment, with a particular focus on Lp(a). We conducted a retrospective cohort study of consecutive hospitalized adults with a first ACS undergoing percutaneous coronary intervention between January 2025 and April 2026. The primary endpoint was attainment of the guideline-recommended LDL-C target at early follow-up, defined as LDL-C < 55 mg/dL and a ≥ 50% reduction from baseline. Associations between clinical variables and LDL-C target attainment were assessed using multivariable logistic regression. Eighty-two patients were included; 70.7% were male and 37.2% had elevated Lp(a) levels. At a median follow-up of 5 weeks (IQR, 4-6), 31.7% attained the LDL-C target despite prescription of high-intensity statin therapy at discharge. In the multivariable model, low Lp(a) (OR 8.72; 95% CI 2.04-37.33), current smoking (OR 5.29; 95% CI 1.42-19.69), and ezetimibe use in addition to high-intensity statin therapy at discharge (OR 5.28; 95% CI 1.31-21.32) were associated with LDL-C target attainment. Early LDL-C target attainment after a first ACS remained limited despite routine prescription of high-intensity statin therapy. Elevated Lp(a) was associated with a lower likelihood of attaining the LDL-C target. Prospective studies are needed to confirm these findings.

PMID 42876442
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PubMedCureus2026-10-15

Persistent HyperCKemia Beyond Post-Viral Myositis: A Case of Anti-HMGCR Immune-Mediated Necrotizing Myopathy.

Xavier Rita R, Silva Sara S, Cunha Rita R, Coelho Angela A et al.

Anti-3-hydroxy-3-methylglutaryl-coenzyme A reductase (anti-HMGCR) immune-mediated necrotizing myopathy (IMNM) is a rare autoimmune myopathy that should be suspected in patients with progressive proximal muscle weakness and marked creatine kinase (CK) elevation persisting despite statin discontinuation, although distinguishing it from more common conditions such as post-viral myositis and toxic statin-associated myopathy remains a major diagnostic challenge. We report the case of a 64-year-old man receiving long-term atorvastatin therapy who presented with progressive proximal muscle weakness, dysphagia, and severe hyperCKemia following a self-limited flu-like illness, initially raising post-viral myositis as the leading hypothesis. Despite immediate statin discontinuation and aggressive intravenous hydration, severe hyperCKemia persisted during the first week of supportive management alone, and the neurological deficits did not improve, prompting further investigation and empirical immunosuppression. Muscle magnetic resonance imaging demonstrated multifocal inflammatory muscle edema, while extensive investigation for infectious, metabolic, endocrine, neoplastic, and autoimmune causes was unrevealing. Muscle biopsy showed a necrotizing myopathy with pauci-inflammatory features, and anti-HMGCR antibodies, which had not been included in the initial extended myositis panel and required a dedicated request, were subsequently identified, confirming statin-associated IMNM. Treatment with high-dose corticosteroids followed by methotrexate produced progressive biochemical improvement and complete recovery of muscle strength and swallowing function, with CK falling to 376 U/L (N 30-200 U/L) at the last follow-up (four months after admission). The principal educational value of this case lies in the diagnostic reasoning rather than in the diagnosis itself: it was the failure of the clinical and biochemical course to follow the anticipated trajectory, rather than the initial presentation, that prompted reconsideration of the working hypothesis. Dysphagia, less commonly reported in post-viral myositis and toxic statin-associated myopathy, together with persistent severe hyperCKemia despite statin withdrawal, should prompt evaluation for anti-HMGCR IMNM.

PMID 42877551
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PubMedFrontiers in cardiovascular medicine2026-10-14

Effect of rosuvastatin and ezetimibe therapy on LDL-cholesterol reduction and non-invasive arterial injury markers in children with heterozygous familial hypercholesterolemia: a prospective, open-label, randomized study.

Skarlovnik Ajda A, Gorjanc Tevz T, Sikonja Jaka J, Kafol Jan J et al.

Individuals with familial hypercholesterolemia (FH) require early lipid-lowering therapy (LLT). We compared rosuvastatin versus ezetimibe treatment and the role of major non-invasive arterial injury markers in children with heterozygous FH. In this prospective, open-label, randomized study, 45 children with FH [median age 10.5 years (IQR 8.7-14.5)] received rosuvastatin 5 mg OD or ezetimibe 10 mg OD for 6.2 months. Carotid intima-media thickness (cIMT), reactive hyperemia index (RHI), pulse wave velocity (PWV), and beta stiffness were evaluated in relation to anthropometric and lipid-related variables. Rosuvastatin produced a greater LDL-C reduction than ezetimibe (36.7% vs. 18.3%; p < 0.001) with 9/20 (45%) children achieving LDL-C <3.5 mmol/L compared to 2/15 (13%) in ezetimibe group. No reports of myalgias, elevations in transaminases, or creatine kinase (CK) were observed in any of the groups. Markers at baseline correlated mainly with age and anthropometry. Beta stiffness decreased during LLT in the overall cohort (-0.24; 95% CI -0.51 to -0.03, p = 0.002) and in the rosuvastatin group (-0.4; 95% CI -0.7 to -0.1, p = 0.028), with no between-group difference (p = 0.266). This likely reflects regression to the mean, as LDL-C reduction and treatment allocation had only small effects across all markers. Rosuvastatin achieved greater LDL-C reduction than ezetimibe in children with FH, without difference in safety and tolerability profiles. Arterial injury markers correlated mainly with age and anthropometry, and their short-term changes were not treatment-related, likely due to limited power and the short follow-up.

PMID 42870880
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