@book{oai:kanazawa-u.repo.nii.ac.jp:00014289,
 author = {Inazu, Akihiro},
 month = {Nov},
 note = {Naturally CETP-deficient animals and genetic cholesteryl ester transfer protein (CETP) deficiency caused by TaqIB polymorphism in human are relatively resistant to atherosclerosis including coronary artery disease (CAD). CETP inhibitors were developed for new therapeutic measures against atherosclerotic vascular disease through increasing high-density lipoprotein cholesterol (HDL-C) and decreasing low-density lipoprotein cholesterol (LDL-C). Although a clinical trial with torcetrapib was terminated due to hypertension-related side effects, two other compounds, anacetrapib and evacetrapib, are under Phase III clinical trials. Although additional failure of dalcetrapib suggested that the hypertension-related adverse effect is not only the cause of failure of torcetrapib, but also the validity of the CETP inhibitor itself is questionable, this chapter summarizes that a hope remains in CETP inhibitors as a potential agent to reduce residual CAD risk in some clinical settings. Rationale for the CETP inhibitor development is discussed from clinical and experimental insights of lipoprotein phenotype, functional activity on LDL and HDL, and role of CETP activity in relation to inflammation. Structure and function relationship between the N-terminal hydrophobic tunnel of CETP and cholesteryl ester (CE)/triglycerides (TG) with or without a CETP inhibitor is discussed. CETP antibody may have a differential potential on directional selectivity of neutral lipid transfer in plasma lipoproteins. © 2014 Elsevier Inc. All rights reserved., [Book Chapter]},
 publisher = {Elsevier},
 title = {Cholesteryl Ester Transfer Protein Inhibitors: A Hope Remains},
 year = {2013}
}