Anacetrapib 是一种有效的 CETP 抑制剂，作用于 rhCETP 和 C13S CETP 突变型，IC₅₀ 分别为 7.9±2.5 nM 和 11.8±1.9 nM。

Anacetrapib is a potent CETP inhibitor, with IC 50 s of 7.9±2.5 nM and 11.8±1.9 nM for rhCETP and C13S CETP mutant, respectively.

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IC50: 7.9±2.5 nM (rhCETP), 11.8±1.9 nM (CETP)

Anacetrapib dose-dependently and significantly decreases the transfer of CE from HDL3 to HDL2 (P<0.001 for concentrations equal to and higher than 0.1 μM). Excess Anacetrapib (25 μM) decreases the amount of [C]Torcetrapib (0.25 μM) binds to immobilized rhCETP by 82% and 60%, respectively. Anacetrapib decreases pre-β-HDL formation by more than 46% (P<0.001) at all concentrations tested (0.1, 1, 3, and 10 μM). A significant reduction of PCSK9 promoter activity by Anacetrapib (ANA) is detected at 3 μM concentration (?22%, p<0.01) and further lowered to 68% of control at 10 μM. Likewise, luciferase activity of B11 cells are decreased by Anacetrapib at 3 μM concentration and reached to a maximal reduction of 38% of control at 10 μM. At 10 μM concentration, Anacetrapib loweres PCSK9 mRNA level to 60% of control and LDLR mRNA level to 67% of control.

Hamsters are given Anacetrapib for 7 days before injection of [H]cholesterol-labeled macrophages (day 0). Treatment with Anacetrapib leads to significant increases in HDL-C levels at day 0. At day 3, [H]cholesterol radioactivity in the HDL fraction is significantly increased from control values for Anacetrapib. Anacetrapib (ANA) treatment modestly elevates serum total serum cholesterol levels ~10% (p<0.05) and increases serum LDL-C by 26% (p<0.05) as compared to vehicle control. After an intravenous dose of 0.5 mg/kg, the mean values for systemic plasma clearance, steady-state volume of distribution, and terminal half-life are 2.3 mL/min/kg, 1.1 L/kg, and 12 h, respectively. After oral dosing at 5 mg/kg, the bioavailability of Anacetrapib is 38%. Exposures (AUC) increases in a less than dose-proportional manner from 23 μM?h at 5 mg/kg to 362 μM?h at 500 mg/kg. In this do

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[1]. Niesor EJ, et al. Modulating cholesteryl ester transfer protein activity maintains efficient pre-β-HDL formation and increases reverse cholesterol transport. J Lipid Res. 2010, 51(12), 3443-3454.
[2]. Dong B, et al. CETP inhibitors downregulate hepatic LDL receptor and PCSK9 expression in vitro and in vivo through a SREBP2 dependent mechanism. Atherosclerosis. 2014 Aug;235(2):449-62.

In Vitro: DMSO : ≥ 100 mg/mL (156.86 mM)配制储备液