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The hypolipidemic therapy is one of the essential components for the management of patients with cardiovascular diseases (CVD). In this regard, the main task of modern research is to find new targets for creating additional effective groups of lipid-lowering drugs. In 2003, a Canadian and French research team led by N. Seidah and M. Abifadel discovered a new enzyme, proprotein convertase subtilisin-kexin type 9 (PCSK9), which plays an important role in lipid metabolism.&#x0D;The main mechanism of action of PCSK9 is to regulate the density of low-density lipoprotein receptors (LDLR) in the cell membrane of hepatocytes. The increased activity of PCSK9 significantly accelerates the degradation of LDLR and leads to an increase in the concentration of atherogenic classes of lipoproteins  the low-density lipoproteins (LDL). A reduced activity of PCSK9, on the contrary, is accompanied by a decrease in the concentration of LDL and a decrease in the risk of developing atherosclerosis and CVD. The second, recently discovered and less studied, mechanism of the protearogenic action of PCSK9 is the enhancement of inflammatory processes in the atherosclerotic plaque. Given this unfavorable contribution of PCSK9 to the development and progression of atherosclerosis and CVD, the main task of the researchers was to develop drugs that inhibit this enzyme. To date, several new drug groups have been developed that target the biosynthesis steps and the function of PCSK9.&#x0D;In this article, we will focus in detail on the discussion of the mechanisms of action and effectiveness of the following groups of lipid-lowering drugs: anti-PCSK9 monoclonal antibodies (alirocumab, evolocumab), small interfering ribonucleic acids (incliciran) and antisense nucleotides.

New groups of hypolipidemic drugs based on inhibition of proprotein convertase subtilisin/kexin type 9 (PCSK9). Part 1