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Monoclonal Antibodies, Gene Silencing and Gene Editing (CRISPR) Therapies for the Treatment of Hyperlipidemia-The Future Is Here

Journal

PHARMACEUTICS
Volume 15, Issue 2, Pages -

Publisher

MDPI
DOI: 10.3390/pharmaceutics15020459

Keywords

atherosclerotic cardiovascular disease; cardiovascular prevention; hyperlipidemia; hypertriglyceridemia; lipoprotein (a)

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This article provides an update on the use of monoclonal antibodies, gene silencing therapies, and gene editing techniques for the management of hyperlipidemia. It reviews the cutting-edge pharmaceuticals targeting LDL cholesterol, PCSK9, lipoprotein (a), angiopoietin-like 3, and apolipoprotein C3. The available and upcoming biotechnological lipid therapies are discussed for clinicians managing patients with familial hyperlipidemia, statin intolerance, hypertriglyceridemia, or elevated lipoprotein (a) levels.
Hyperlipidemia is a significant risk factor for atherosclerotic cardiovascular disease. Undertreatment of elevated lipids persists despite existing therapies. Here, we provide an update on monoclonal antibodies, gene silencing therapies, and gene editing techniques for the management of hyperlipidemia. The current era of cutting-edge pharmaceuticals targeting low density lipoprotein cholesterol, PCSK9, lipoprotein (a), angiopoietin-like 3, and apolipoprotein C3 are reviewed. We outline what is known, studies in progress, and futuristic goals. This review of available and upcoming biotechnological lipid therapies is presented for clinicians managing patients with familial hyperlipidemia, statin intolerance, hypertriglyceridemia, or elevated lipoprotein (a) levels.

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