Preprint Review Version 1 Preserved in Portico This version is not peer-reviewed

PCSK9 Inhibitors: Pharmacology and Therapeutic Potential

Version 1 : Received: 21 May 2022 / Approved: 23 May 2022 / Online: 23 May 2022 (10:01:24 CEST)

How to cite: Singh, K.; Gupta, J.K.; Kumar, S.; Singh, K.; Meenakshi, K.; Kumar, K. PCSK9 Inhibitors: Pharmacology and Therapeutic Potential. Preprints 2022, 2022050290. https://doi.org/10.20944/preprints202205.0290.v1 Singh, K.; Gupta, J.K.; Kumar, S.; Singh, K.; Meenakshi, K.; Kumar, K. PCSK9 Inhibitors: Pharmacology and Therapeutic Potential. Preprints 2022, 2022050290. https://doi.org/10.20944/preprints202205.0290.v1

Abstract

Proprotein convertase subtilisin/Kexin type 9 (PCSK9) is a proteolytic enzyme that indirectly regulates serum LDL cholesterol by destroying LDL receptors. In clinical studies, the main role of the proprotein convertase subtilisin/Kexin type9 (PCSK9) inhibitor in cholesterol regulation was elucidated. It is produced in the liver but is also present in the kidney and intestine. It prevents HMGCo from synthesizing cholesterol. SREBP-2 is a reductase that is induced by statins. In a dose-dependent manner, increasing SREBP-2 levels enhanced LDL-R and PCSK9 gene expression. At the minimum, two procedures have been developed to overcome the plasma level of PCSK9. This is the LDLR test, polyclonal antibodies, and sentience oligonucleotide. Lower dosage statin treatment with a proprotein convertase subtilisin/Kexin type9 inhibitor will be most efficient in lowering LDL and avoiding statin adverse effects. In multiple long-term trials, statins have been found to reduce cardiovascular mortality by 30% and stroke incidence by 20%. In this way, we conclude the role of PCSK9 in hypercholesterolemia.

Keywords

Cholesterol; PCSK9 inhibitors; HMG-CoA; LDL receptor; statins

Subject

Biology and Life Sciences, Immunology and Microbiology

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