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Global Translational Medicine Anti-inflammatory therapy in CVD

Figure 2. Pathophysiology and pharmacological interventions in atherosclerosis. This detailed diagram illustrates the key mechanisms in the development
of atherosclerosis, highlighting the role of lipid accumulation, immune cell activation, and smooth muscle proliferation in plaque formation. It also
presents various therapeutic strategies, including statins, HDL modification, gene therapy, bempedoic acid, eicosapentaenoic acid (EPA), and newer
medications, such as ezetimibe and proprotein convertase subtilisin/kexin type 9 (PCSK9) inhibitors. Image created by the authors with notability.
Abbreviations: CETP: Cholesteryl ester transfer protein; HDL: High-density lipoprotein; HMG-CoA reductase: 3-hydroxy-3-methylglutaryl-coenzyme A
reductase; IFN-gamma: Interferon-gamma; IL: Interleukin; LDL: Low-density lipoprotein; MCP-1: Monocyte chemoattractant protein 1; NF-κB: Nuclear
factor kappa B; NPC1L1: Niemann–Pick C1-like protein 1; TNF-alpha: Tumor necrosis factor-alpha.

Obicetrapib, a newer CETP inhibitor, has shown pre-β HDL, mature HDL particles, and ApoA1. In phase 2
improved safety and efficacy compared to previous agents. trials, the 10 mg obicetrapib group showed a 45% median
It significantly lowers the levels of LDL, non-HDL, ApoB, reduction in LDL levels, a 34% reduction in ApoB levels,
and lipoprotein (Lp[a]) while increasing the levels of and a 33% decrease in Lp(a) levels. Obicetrapib’s clinical
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Volume 4 Issue 3 (2025) 15 doi: 10.36922/GTM025100024