Cholesteryl ester transfer protein (CETP) is a plasma glycoprotein that promotes reverse cholesterol transport via the exchange of cholesteryl ester (CE) and triglyceride (TG) among lipoproteins. Cholesteryl ester transfer protein (CETP) promotes reverse cholesterol transport via exchange of cholesteryl ester and triglyceride among lipoproteins. CETP has a central role in lipoprotein metabolism.
CETP, a hydrophobic plasma glycoprotein, is a promising target for raising circulating HDL cholesterol (HDL-C) concentrations in humans. CETP is secreted primarily from the liver and plays a critical role in HDL metabolism by facilitating the exchange of cholesteryl esters (CE) from HDL for triglycerides (TG) in apoB-containing lipoproteins, such as LDL and VLDL.
CETP catalyses the exchange of cholesteryl ester and triglyceride between HDL and apoB containing lipoprotein particles. The role of CETP in modulating plasma HDL cholesterol levels in humans is well established and there have been significant efforts to develop CETP inhibitors to increase HDL cholesterol for the treatment of coronary artery disease.
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Anacetrapib (MK 0859) is a potent, orally active cholesteryl ester transfer protein (CETP) inhibitor with IC50 of 7.9 nM and 11.8 nM for rhCETP and C13S CETP mutant, respectively; inhibits CETP-mediated cholesterol exchange, resulting in elevated HDL-cholesterol levels and reductions in LDL-cholesterol levels, demonstrates potential to treat elevated cholesterol levels in an effort prevent cardiovascular disease.
Torcetrapib (CP-529414) is a potent cholesteryl ester transfer protein (CETP) inhibitor with IC50 of 37 nM; shows the potential to treat hypercholesterolemia (elevated cholesterol levels) and prevent cardiovascular disease.
TAP-311(TAP311) is a novel potent and selective CETP inhibitor with plasma IC50 of 62 nM; displays >170-fold selectivity over CYPs, and has excellent pharmacokinetics in rats and robust efficacy in hamsters; shows substantially reduced lipophilicity with only modest distribution into adipose tissue, and retains potency in hypertriglyceridemic plasma in vitro and in vivo; does not increase blood pressure or plasma aldosterone levels in vivo, in contrast to torcetrapib.
Obicetrapib (AMG-899, TA-8995, DEX-001) is a potent, ora cholesteryl ester transfer protein (CETP) inhibitor for treatment of dyslipidaemia.
Evacetrapib (LY2484595) is a potent and selective inhibitor of cholesteryl ester transfer protein (CETP) with IC50 of 5.5 nM for human recombinant CETP protein; inhibits CETP activity in human plasma with IC50 of 36 nM; shows no significant inhibition in the CEREP cell surface receptor screening, as well as the nuclear receptor panel; exhibits an ex vivo CETP inhibition ED50 of < 5 mg/kg at 8 h post oral dose and significantly elevates HDL cholesterol in vivo; Evacetrapib is a potent and selective CETP inhibitor without torcetrapib-like off-target liabilities.
Rocacetrapib (CKD-519, CKD519) is a potent, selective cholesteryl ester transfer protein (CETP) inhibitor, inhibits the CETP-mediated transfer of cholesteryl ester in human serum with IC50 of 2.3 nM; exhibites a maximum of 70%-86% inhibition of CETP activity and 25%-48% increase of HDL-C levels after two weeks of oral administration of 1, 3, or 10 mg/kg in transgenic mice expressing human CETP/apolipoprotein AI; CKD-519 (Rocacetrapib, CKD519) is being developed for the treatment of dyslipidemia to raise high-density lipoprotein cholesterol.
BMS-795311(BMS795311) is a potent and orally available CETP inhibitor with IC50 of 3.8 nM, inhibits cholesteryl ester (CE) transfer with IC50 of 0.22 uM; inhibits CE transfer activity at an oral dose of 1 mg/kg in human CETP/apoB-100 dual transgenic mice and increased HDL cholesterol content and size comparable to Torcetrapib in moderately-fat fed hamsters.
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