BMS-795311 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.
CETP-IN-3 (Compound 13) is an small molecule inhibitor of the plasma glycoprotein cholesterol ester transfer protein (CETP), elevating HDL-C through inhibition of CETP. CETP-IN-3 for the CETP inhibitory activity in the scintillation proximity (SPA) and whole plasma assay (WPA) with IC50s of 0.002 μM and 0.06 μM, respectively[1].
Rosenonolactone shows inhibitory activity against prolyl endopeptidase and thrombin and cholesterol ester transfer protein[1][2][3].
Evacetrapib is a potent and selective of CETP inhibitor, which inhibits human recombinant CETP protein (IC50 5.5 nM) and CETP activity in human plasma (IC50 36 nM) in vitro.
Anacetrapib is a potent CETP inhibitor, with IC50s of 7.9±2.5 nM and 11.8±1.9 nM for rhCETP and C13S CETP mutant, respectively.
Torcetrapib(CP-529414) is a CETP inhibitor with IC50 of 37 nM, elevates HDL-C and reduces nonHDL-C in plasma.IC50 value: 37 nM [1]Target: CETP inhibitorin vitro: Torcetrapib dose-dependently increases aldosterone release from H295R cells after either 24 or 48 h of treatment with an EC50 of approximately 80 nM, this effect is mediated by calcium channel as calcium channel blockers completely blocks torcetrapib-induced corticoid release and calcium increase. Torcetrapib (1 μM) significantly increases the expression of steroidogenic gene, CYP11B2 and CYP11B1, in H295R cell lines [2].in vivo: Torcetrapib (< 100 mg, daily) changes the plasma distribution of CETP, as the apparent molecular weight of the CETP has shifted to a larger form, by 2 hours after the dose in healthy young subjects. Torcetrapib treatment with 10 mg, 30 mg, 60 mg, and 120 mg daily and 120 mg twice daily results in 16%, 28%, 62%, 73%, and 91% increases in plasma HDL-C, respectively, with no significant changes in TPC in healthy young subjects. [1] Torcetrapib results in an increase of 72.1% in high-density lipoprotein cholesterol and a decrease of 24.9% in low-density lipoprotein cholesterol, in addition to an increase of 5.4 mm Hg in systolic blood pressure, a decrease in serum potassium, and increases in serum sodium, bicarbonate, and aldosterone, in patients at high cardiovascular risk after 12 months' treatment [3]. Torcetrapib (90 mg/kg/day) results in a 70% inhibition of CE transfer in rabbits fed an atherogenic diet. Torcetrapib (90 mg/kg/day) increases mean HDL-C levels by above 3-fold and apoA-I levels by 2.5-fold in plasma in rabbits fed an atherogenic diet. Torcetrapib-treated animal has a multiple-fold increase in HDL-C AUC and a corresponding reduction in aortic lesion area with 60% reduction of aortic free cholesterol (FC) and cholesteryl ester (EC) in rabbits fed an atherogenic diet. Torcetrapib-treated rabbits stimulate free cholesterol efflux to a significantly greater extent than does sera from control rabbits [4].
CETP-IN-4 is a cholesteryl ester transfer protein (CETP) inhibitor.
CP-532623 is a CETP inhibitor and elevates high-density lipoprotein cholesterolion. CP-532623 is a close structural analogue of Torcetrapib. CP-532623 has highly lipophilic properties[1][2][3].
Dalcetrapib (JTT-705; RO-4607381) is a rhCETP inhibitor with IC50 of 0.2 μM that increases the plasma HDL cholesterol. IC50 value: 0.2 uM [1]Target: CETPin vitro: Dalcetrapib modulates CETP activity. Dalcetrapib induces a conformational change in CETP, when added to human plasma. CETP-induced pre-β-HDL formation in human plasma is unchanged by Dalcetrapib ≤3 μM and increased at 10 μM. Dalcetrapib statistically and significantly increases pre-β-HDL formation [1]. Dalcetrapib achieves 50% inhibition of CETP activity in human plasma at a concentration of 9 μM [2]. Dalcetrapib inhibits the CETP activity of media in HepG2 in a dose-dependent manner [3].in vivo: Treatment with Dalcetrapib leads to significant increases in HDL-C levels. In hamsters injected with [3H]cholesterol-labeled autologous macrophages Dalcetrapib significantly increases fecal elimination of both [3H]neutral sterols and [3H]bile acids. Dalcetrapib increases plasma HDL-[3H]cholesterol [1]. Dalcetrapib has 95% inhibition of CETP activity in male Japanese white rabbits at an oral dose of 30 mg/kg. Dalcetrapib increases the plasma HDL cholesterol level by 27% and 54%, respectively, when given at oral doses of 30 mg/kg or 100 mg/kg once a day for 3 days to male Japanese white rabbits [2].
MK-8262 is an orally active and potent cholesteryl ester transfer protein (CETP) inhibitor with an IC50 of 53 nM and a log D of 5.3. MK-8262, a bistrifluoromethyl analogue, has the potential for coronary heart disease (CHD) correlated high-density lipoprotein (HDL) and low-density lipoprotein (LDL) research[1].
CKD-519 is a selective and potent cholesteryl ester transfer protein (CETP) inhibitor, which inhibits CETP-mediated transfer of cholesteryl ester in human serum with an IC50 of 2.3 nM[1].