Novel lecithin: cholesterol acyltransferase-based therapeutic approaches
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Updated: Dec 28, 2025

A Familial Hypercholesterolemia Human Liver Chimeric Mouse Model Using Induced Pluripotent Stem Cell-derived Hepatocytes
Published on: September 15, 2018
Lita A Freeman1, Sotirios K Karathanasis1,2, Alan T Remaley1
1Lipoprotein Metabolism Laboratory, Translational Vascular Medicine Branch, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda.
Purpose Of Review:
To review recent lecithin:cholesterol acyltransferas (LCAT)-based therapeutic approaches for atherosclerosis, acute coronary syndrome, and LCAT deficiency disorders.
Recent Findings:
A wide variety of approaches to using LCAT as a novel therapeutic target have been proposed. Enzyme replacement therapy with recombinant human LCAT is the most clinically advanced therapy for atherosclerosis and familial LCAT deficiency (FLD), with Phase I and Phase 2A clinical trials recently completed. Liver-directed LCAT gene therapy and engineered cell therapies are also another promising approach. Peptide and small molecule activators have shown efficacy in early-stage preclinical studies. Finally, lifestyle modifications, such as fat-restricted diets, cessation of cigarette smoking, and a diet rich in antioxidants may potentially suppress lipoprotein abnormalities in FLD patients and help preserve LCAT activity and renal function but have not been adequately tested.
Summary:
Preclinical and early-stage clinical trials demonstrate the promise of novel LCAT therapies as HDL-raising agents that may be used to treat not only FLD but potentially also atherosclerosis and other disorders with low or dysfunctional HDL.
Insights
Novel lecithin:cholesterol acyltransferase (LCAT) therapies show promise for treating familial LCAT deficiency (FLD), atherosclerosis, and cardiovascular conditions by raising HDL levels. Enzyme replacement and gene therapies are advancing, with early trials showing positive results.
Area of Science:
- Biochemistry
- Cardiovascular Medicine
- Genetics
Background:
- Lecithin:cholesterol acyltransferase (LCAT) plays a crucial role in high-density lipoprotein (HDL) metabolism.
- Dysfunctional LCAT activity is implicated in familial LCAT deficiency (FLD) and contributes to cardiovascular disease.
- Novel therapeutic strategies targeting LCAT are being explored to address these conditions.
Purpose of the Study:
- To review recent advancements in lecithin:cholesterol acyltransferase (LCAT)-based therapeutic approaches.
- To evaluate LCAT-based therapies for atherosclerosis, acute coronary syndrome, and LCAT deficiency disorders.
Main Methods:
- Review of recent preclinical and clinical trial data on LCAT-based therapies.
- Analysis of enzyme replacement therapy, gene therapy, engineered cell therapies, and small molecule activators.
- Consideration of lifestyle modifications for managing LCAT deficiency.
Main Results:
- Enzyme replacement therapy with recombinant human LCAT is clinically advanced, with completed Phase I and 2A trials.
- Liver-directed LCAT gene therapy and engineered cell therapies represent promising alternative approaches.
- Peptide and small molecule LCAT activators have demonstrated efficacy in early preclinical studies.
- Lifestyle modifications may help manage FLD but require further investigation.
Conclusions:
- Novel LCAT therapies demonstrate potential as HDL-raising agents.
- These therapies may be beneficial for treating familial LCAT deficiency (FLD).
- LCAT-based treatments could also be applicable to atherosclerosis and other disorders characterized by low or dysfunctional HDL.
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