Evacetrapib

Research use only, not for human use.

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.

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.Dyslipidemia Discontinued(In Vitro):Evacetrapib is a novel benzazepine-based CETP inhibitor. In the buffer CETP assay, the absolute potency of the compound is 5.5 nM. In the human plasma CETP assay, the CETP concentration is about 2 μg/mL (25 nM) and the 36 nM IC50 value again indicates that Evacetrapib is a potent CETP inhibitor against either the recombinant protein or CETP from human plasma. Evacetrapib is apparently much more potent than Dalcetrapib.(In Vivo):In double transgenic mice expressing human CETP and apoAI, Evacetrapib exhibits an ex vivo CETP inhibition ED50 of less than 5 mg/kg at 8 h post oral dose and significantly elevated HDL cholesterol. Importantly, no blood pressure elevation is observed in rats dosed with Evacetrapib at high exposure multiples compared with the positive control, torcetrapib. Evacetrapib administered orally at 30 mg/kg results in 98.4%, 98.6%, and 18.4% inhibition of CETP activity at 4, 8 and 24 h post dose respectively. Evacetrapib dosed orally at 30 mg/kg resulted in 129.7% increase in HDL-C 8 h after oral administration.

Evacetrapib is a novel benzazepine-based CETP inhibitor. In the buffer CETP assay, the absolute potency of the compound is 5.5 nM. In the human plasma CETP assay, the CETP concentration is about 2 μg/mL (25 nM) and the 36 nM IC50 value again indicates that Evacetrapib is a potent CETP inhibitor against either the recombinant protein or CETP from human plasma. Evacetrapib is apparently much more potent than Dalcetrapib.

In double transgenic mice expressing human CETP and apoAI, Evacetrapib exhibits an ex vivo CETP inhibition ED50 of less than 5 mg/kg at 8 h post oral dose and significantly elevated HDL cholesterol. Importantly, no blood pressure elevation is observed in rats dosed with Evacetrapib at high exposure multiples compared with the positive control, torcetrapib. Evacetrapib administered orally at 30 mg/kg results in 98.4%, 98.6%, and 18.4% inhibition of CETP activity at 4, 8 and 24 h post dose respectively. Evacetrapib dosed orally at 30 mg/kg resulted in 129.7% increase in HDL-C 8 h after oral administration.

LY2484595 | LY 2484595 | LY-2484595

Metabolic Enzyme/Protease

CETP

CETP

Cardiovascular Disease

Dyslipidemia

1186486-62-3

638.7

C31H36F6N6O2

>98% (HPLC)

10 mM in DMSO

O=C([C@H]1CC[C@H](CN2C3=C(C)C=C(C)C=C3[C@@H](N(CC4=CC(C(F)(F)F)=CC(C(F)(F)F)=C4)C5=NN(C)N=N5)CCC2)CC1)O

Cyclohexanecarboxylic acid, 4-[[(5S)-5-[[[3,5-bis(trifluoromethyl)phenyl]methyl](2-methyl-2H-tetrazol-5-yl)amino]-2,3,4,5-tetrahydro-7,9-dimethyl-1H-1-benzazepin-1-yl]methyl]-, trans-

(-20℃)

With Ice Pack

≥ 2 years