Trial reportArteriosclerosis, thrombosis, and vascular biology2018
CSL112 (Apolipoprotein A-I [Human]) Enhances Cholesterol Efflux Similarly in Healthy Individuals and Stable Atherosclerotic Disease Patients.
Trial report in Arteriosclerosis, thrombosis, and vascular biology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
35 citing papers in PubMed, 1 synthesis or guideline pooled it, 65 citations in OpenAlex.
- Cholesterol Efflux Capacity and Its Association With Adverse Cardiovascular Events: A Systematic Review and Meta-Analysis.Frontiers in cardiovascular medicine · 2021Pooled it
- Effect of CSL112 (apolipoprotein A-I [human]) on cholesterol efflux capacity in Japanese subjects: Findings from a phase I study and a cross-study comparison.Clinical and translational science · 2022Trial
- Trial
- Pharmacometric analyses to characterize the effect of CSL112 on apolipoprotein A-I and cholesterol efflux capacity in acute myocardial infarction patients.British journal of clinical pharmacology · 2021Trial
- Inventive HDL Mimicking Nanoparticles: A Promising Frontier in Cardiovascular Disease Management.Cardiovascular toxicology · 2025Review
- Apolipoprotein A1 (CSL112) Increases Lecithin-Cholesterol Acyltransferase Levels in HDL Particles and Promotes Reverse Cholesterol Transport.JACC. Basic to translational science · 2025Article
- HDL-replacement therapy: From traditional to emerging clinical applications.Atherosclerosis plus · 2025Review
- High-density lipoprotein in diabetes: Structural and functional relevance.Journal of diabetes investigation · 2024Review
- Recent advances of self-assembled nanoparticles in the diagnosis and treatment of atherosclerosis.Theranostics · 2024Review
- Biological basis and proposed mechanism of action of CSL112 (apolipoprotein A-I [human]) for prevention of major adverse cardiovascular events in patients with myocardial infarction.European heart journal. Cardiovascular pharmacotherapy · 2023Review
- A Current Update on the Role of HDL-Based Nanomedicine in Targeting Macrophages in Cardiovascular Disease.Pharmaceutics · 2023Review
- N-terminal eGFP-tagging of rabbit apolipoprotein A-I decreases expression and impairs cholesterol-efflux activity.Biochimica et biophysica acta. Molecular and cell biology of lipids · 2023Article
- Clinical Pharmacokinetics and Pharmacodynamics of CSL112.Clinical pharmacokinetics · 2023Review
- HDL-Based Therapy: Vascular Protection at All Stages.Biomedicines · 2023Review
- Genetic and observational evidence: No independent role for cholesterol efflux over static high-density lipoprotein concentration measures in coronary heart disease risk assessment.Journal of internal medicine · 2022Observational
- ApoA-I Infusion Therapies Following Acute Coronary Syndrome: Past, Present, and Future.Current atherosclerosis reports · 2022Review
- Antiatherosclerotic Effects of CSL112 Mediated by Enhanced Cholesterol Efflux Capacity.Journal of the American Heart Association · 2022Review
- HDL Is Not Dead Yet.Biomedicines · 2022Review
- High-density lipoproteins, reverse cholesterol transport and atherogenesis.Nature reviews. Cardiology · 2021Review
- Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveCSL112 (apolipoprotein A-I [apoA-I; human]) is a novel formulation of apoA-I in development for reduction of early recurrent cardiovascular events after acute myocardial infarction. Cholesterol efflux capacity (CEC) is a marker of high-density lipoprotein (HDL) function that is strongly correlated with incident cardiovascular disease. Impaired CEC has been observed in patients with coronary heart disease. Here, we determined whether infused apoA-I improves CEC when administered to patients with stable atherosclerotic disease versus healthy volunteers. APPROACH AND
resultsMeasurements of apoA-I, HDL unesterified cholesterol, HDL esterified cholesterol, pre-β1-HDL, and CEC were determined in samples from patients with stable atherosclerotic disease before and after intravenous administration of CSL112. These measures were compared with 2 prior studies in healthy volunteers for differences in CEC at baseline and after CSL112 infusion. Patients with stable atherosclerotic disease exhibited significantly lower ATP-binding cassette transporter 1-mediated CEC at baseline (
conclusionsCSL112 shows comparable, strong, and immediate effects on CEC despite underlying cardiovascular disease. CSL112 is, therefore, a promising novel therapy for lowering the burden of atherosclerosis and reducing the risk of recurrent cardiovascular events.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.