ezetimibe + rosuvastatin (NVP1205 / NVP 1205)

Suspected Rosuvastatin-Associated Bullous Pemphigoid: A Diagnostic and Therapeutic Challenge.

Gandhi Shirley S, Clark Barrie B, Ashraf Iman I, Qadir Nadim N et al.

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.

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.

Enlicitide: The First Oral PCSK9i for Lowering Low-Density Lipoprotein Cholesterol.

Lucas Rachel C RC, Lussier Mia E ME, Nasuhidehnavi Azadeh A, Clark Taylor M TM

This article describes pharmacology, pharmacokinetics, safety, and efficacy data of enlicitide, the first Food and Drug Administration (FDA)-approved oral proprotein convertase subtilisin/kexin type 9 inhibitor (PCSK9i). PubMed, Embase, Web of Science, and Cochrane were searched through July 17, 2026. Clinical trials published in English were included. Relevant information from the methodology and results was extracted. Enlicitide received FDA approval on July 16, 2026, based on results from phase 2 and 3 trials showing a 57.1% to 64.6% reduction in low-density lipoprotein-cholesterol (LDL-C) and reduced other atherogenic lipid particles at 24 weeks in patients with hypercholesterolemia, including those with heterozygous familial hypercholesterolemia, while maintaining a favorable adverse effect profile. Enlicitide represents the fifth FDA-approved agent targeting PCSK9, having similar efficacy to other agents in class while having a novel macrocyclic peptide formulation with permeation enhancers, allowing for oral administration.Relevance to Patient Care and Clinical Practice in Comparison With Existing Drugs:As PCSK9is continue to be at the forefront of dyslipidemia guidelines, the approval of an oral agent is paramount in ensuring patient access. Enlicitide mirrors LDL-C lowering compared with existing PCSK9is and surpasses LDL-C lowering compared with non-statin options such as bempedoic acid and ezetimibe. Confirmation of cardiovascular outcomes data with enlicitide will solidify its role in reducing atherosclerotic cardiovascular disease risk. Enlicitide significantly lowered LDL-C similar to existing PCSK9is with few adverse effects. The oral formulation provides an essential option for LDL-C lowering, especially in patients adverse to injections.