Claims
- 1. A compound of the formula I, or a pharmaceutically acceptable salt or ester thereof, in whichR1, R2, R3, R4, R5, R6 independently of one another are (C0-C30)-alkylene-L, where one or more carbon atoms of the alkylene radical may be replaced by —O—, —(C═O)—, —CH═CH—, —C≡C—, —N((C1-C6)-alkyl)- or —NH—; or H, F, Cl, Br, I, CF3, NO2, CN, COOH, COO(C1-C6)-alkyl, CONH2, CONH(C1-C6)-alkyl, CON[(C1-C6)-alkyl]2, (C1-C6)-alkyl, (C2-C6)-alkenyl, (C2-C6)-alkynyl or O—(C1-C6)-alkyl, where one or more hydrogens in the alkylene radicals may be replaced by fluorine; or SO2—NH2, SO2NH(C1-C6)-alkyl, SO2N[(C1-C6)-alkyl]2, S—(C1-C6)-alkyl, S—(CH2)n-phenyl, SO—(C1-C6)-alkyl, SO—(CH2)n-phenyl, SO2—(1-C6)-alkyl or SO2—(CH2)n-phenyl, where n=0-6 and the phenyl radical may be substituted up to two times by F, Cl, Br, OH, CF3, NO2, CN, OCF3, O—(C1-C6)-alkyl, (C1-C6)-alkyl or NH2; or NH2, NH—(C1-C6)-alkyl, N((C1-C6)-alkyl)2, NH(C1-C7)-acyl, phenyl or O—(CH2)n-phenyl, where n=0-6, where the phenyl ring may be mono- to trisubstituted by F, Cl, Br, I, OH, CF3, NO2, CN, OCF3, O—(C1-C6)-alkyl, (C1-C6)-alkyl, NH2, NH(C1-C6)-alkyl, N((C1-C6)-alkyl)2, SO2—CH3, COOH, COO—(C1-C6)-alkyl or CONH2; is shown connected to (C0-C30)-alkylene as follows: R7 is methyl, ethyl, propyl or butyl; R8 is H, OH, NH2 or NH—(C1-C6)-alkyl; R9 is methyl, ethyl, propyl or butyl; R10 is methyl, ethyl, propyl or butyl; wherein at least one of the radicals R1 to R6 has the meaning (C0-C30)-alkylene-L, where one or more carbon atoms of the alkylene radical may be replaced by —O—, —(C═O)—, —CH═CH—, —C≡C—, —N((C1-C6)-alkyl)- or —NH—.
- 2. A compound as claimed in claim 1, whereinR1, R2, R3, R4, R5, R6 independently of one another are (C0-C30)-alkylene-L, where one or more carbon atoms of the alkylene radical may be replaced by —O—, —(C═O)- or —NH—; or H, F, Cl, Br, I, CF3, NO2, CN, COOH, COO(C1-C6)-alkyl, CONH2, CONH(C1-C6)alkyl, CON[(C1-C6)alkyl]2, (C1-C6)-alkyl, (C2-C6)-alkenyl, (C2-C6)-alkynyl or O—(C1-C6)-alkyl, where one or more hydrogens in the alkylene radicals may be replaced by fluorine; or SO2—NH2, SO2NH(C1-C6)-alkyl, SO2N[(C1-C6)-alkyl]2, S—(C1-C6)-alkyl, S—(CH2)n-phenyl, SO—(C1-C6)-alkyl, SO—(CH2)n-phenyl, SO2—(C1-C6)-alkyl or SO2—(H2)n-phenyl, where n=0-6 and the phenyl radical may be substituted up to two times by F, Cl, Br, OH, CF3, NO2, CN, OCF3, O—(C1-C6)-alkyl, (C1-C6)-alkyl or NH2; or NH2, NH—(C1-C6)-alkyl, N((C1-C6)-alkyl)2, NH(C1-C7)-acyl, phenyl or O—(CH2)n-phenyl, where n=0-6, where the phenyl ring may be mono- to trisubstituted by F, Cl, Br, I, OH, CF3, NO2, CN, OCF3, O—(C1-C6)-alkyl, (C1-C6)-alkyl, NH2, NH(C1-C6)-alkyl, N((C1-C6)-alkyl)2, SO2—CH3, COOH, COO—(C1-C6)-alkyl or CONH2; is shown connected to (C0-C30)-alkylene as follows: R7 is methyl, ethyl, propyl or butyl; R8 is H, OH, NH2 or NH—(C1-C6)-alkyl; R9 is methyl, ethyl, propyl or butyl; R10 is methyl, ethyl, propyl or butyl; wherein at least one of the radicals R1 to R6 has the meaning (C0-C30)-alkylene-L, where one or more carbon atoms of the alkylene radical may be replaced by —O—, —(C═O)- or —NH—.
- 3. A compound as claimed in claim 1, whereinR1, R2, R3, R4, R5, R6 independently of one another are (C0-C30)-alkylene-L, where one or more carbon atoms of the alkylene radical may be replaced by —O—, —(C═O)- or —NH—; or H, F, Cl, Br, I, CF3, NO2, CN, COOH, COO(C1-C6)-alkyl, CONH2, CONH(C1-C6)-alkyl, CON[(C1-C6)-alkyl]2, (C1-C6)-alkyl, (C2-C6)-alkenyl, (C2-C6)-alkynyl or O—(C1-C6)-alkyl, where one or more hydrogens in the alkylene radicals may be replaced by fluorine; or SO2—NH2, SO2NH(C1-C6)-alkyl, SO2N[(C1-C6)-alkyl]2, S—(C1-C6)-alkyl, S—(CH2)n-phenyl, SO—(C1-C6)-alkyl, SO—(CH2)n-phenyl, SO2—(1-C6)-alkyl or SO2—(H2)n-phenyl, where n=0-6 and the phenyl radical may be substituted up to two times by F, Cl, Br, OH, CF3, NO2, CN, OCF3, O—(C1-C6)-alkyl, (C1-C6)-alkyl or NH2; or NH2, NH—(C1-C6)-alkyl, N((C1-C6)-alkyl)2, NH(C1-C7)-acyl, phenyl or O—(CH2)n-phenyl, where n=0-6, where the phenyl ring may be mono- to trisubstituted by F, Cl, Br, I, OH, CF3, NO2, CN, OCF3, O—(C1-C6)-alkyl, (C1-C6)-alkyl, NH2, NH(C1-C6)-alkyl, N((C1-C6)-alkyl)2, SO2—CH3, COOH, COO—(C1-C6)-alkyl or CONH2; is shown connected to (C0-C30)-alkylene as follows: R7 is methyl, ethyl, propyl or butyl; R8 is H, OH, NH2 or NH—(C1-C6)-alkyl; R9 is methyl, ethyl, propyl or butyl; R10 is methyl, ethyl, propyl or butyl; where one of the radicals R1 or R3 has the meaning (C0-C30)-alkylene-L, where one or more carbon atoms of the alkylene radical may be replaced by —O—, —(C═O)- or —NH—.
- 4. A compound as claimed in claim 1, whereinR1, R2, R3, R4, R5, R6 independently of one another are —(CH2)0−1—NH—(C═O)0−1—(C3-C25)-alkylene-(C═O)0−1—NH—L, where one or more carbon atoms of the alkylene radical may be replaced by oxygen atoms; or H, F, Cl, Br, I, CF3, NO2, CN, COOH, COO(C1-C6)-alkyl, CONH2, CONH(C1-C6)-alkyl, CON[(C1-C6)-alkyl]2, (C1-C6)-alkyl, (C2-C6)-alkenyl, (C2-C6)-alkynyl or O—(C1-C6)-alkyl, where one or more hydrogens in the alkylene radicals may be replaced by fluorine; or SO2—NH2, SO2NH(C1-C6)-alkyl, SO2N[(C1-C6)-alkyl]2, S—(C1-C6)-alkyl, S—(CH2)n-phenyl, SO—(C1-C6)-alkyl, SO—(CH2)n-phenyl, SO2—(C1-C6)-alkyl or SO2—(H2)n-phenyl, where n=0-6 and the phenyl radical may be substituted up to two times by F, Cl, Br, OH, CF3, NO2, CN, OCF3, O—(C1-C6)-alkyl, (C1-C6)-alkyl or NH2; or NH2, NH—(C1-C6)-alkyl, N((C1-C6)-alkyl)2, NH(C1-C7)-acyl, phenyl or O—(CH2)n-phenyl, where n=0-6, where the phenyl ring may be mono- to trisubstituted by F, Cl, Br, I, OH, CF3, NO2, CN, OCF3, O—(C1-C6)-alkyl, (C1-C6)-alkyl, NH2, NH(C1-C6)-alkyl, N((C1-C6)-alkyl)2, SO2—CH3, COOH, COO—(C1-C6)-alkyl or CONH2; is shown connected to (C0-C30)-alkylene as follows: R7 is methyl, ethyl, propyl or butyl; R8 is H, OH, NH2 or NH—(C1-C6)-alkyl; R9 is methyl, ethyl, propyl or butyl; R10 is methyl, ethyl, propyl or butyl; where one of the radicals R1 to R3 has the meaning —(CH2)0−1—NH—(C═O)0−1—(C3-C25)-alkylene-(C═O)0−1—NH—L, where one or more carbon atoms of the alkylene radical may be replaced by oxygen atoms.
- 5. A pharmaceutical composition comprising one or more of the compounds as claimed in claim 1 and a pharmaceutically acceptable carrier.
- 6. A pharmaceutical composition comprising one or more compounds as claimed claim 1 and at least one further active compound.
- 7. A pharmaceutical composition as claimed in claim 6, comprising, as a further active compound, one or more compounds that normalize lipid metabolism.
- 8. A pharmaceutical composition as claimed in claim 6, comprising, as a further active compound, one or more antidiabetics, hypoglycemically active compounds, HMGCoA reductase inhibitors, cholesterol absorption inhibitors, PPAR gamma agonists, PPAR alpha agonists, PPAR alpha/gamma agonists, fibrates, MTP inhibitors, bile acid absorption inhibitors, CETP inhibitors, polymeric bile acid adsorbers, LDL receptor inducers, ACAT inhibitors, antioxidants, lipoprotein lipase inhibitors, ATP citrate lyases inhibitors, squalene synthetase inhibitors, lipoprotein(a) antagonists, lipase inhibitors, insulins, sulphonyl ureas, biguanides, meglitinides, thiolidindiones, α-glucosidase inhibitors, active compounds which act on the ATP-dependent potassium channel of the beta cells, CART agonists, NPY agonists, MC4 agonists, orexin agonists, H3 agonists, TNF agonists, CRF agonists, CRF BP agonists, urocortin agonists, β3 agonists, MSH (melanocyte-stimulating hormone) agonists, CCK agonists, serotonin-reuptake inhibitors, mixed serotonin and noradrenergic compounds, 5HT agonists, bombesin agonists, galanin agonists, growth hormones, growth hormone-releasing compounds, TRH agonists, decoupling protein 2- or 3-modulators, leptin agonists, DA agonists, lipase/amylase inhibitors, PPAR modulators, R×R modulators or TR-β-agonists or amphetamines.
- 9. A method for controlling the serum cholesterol concentration in a host, which comprises administering to the host in need of the control of serum cholesterol concentration an effective amount of at least one compound as claimed in claim 1.
- 10. A method for the treatment of at least one disorder selected from impaired lipid metabolism, hyperlipidemia, an arteriosclerotic symptom, and insulin resistance, which comprises administering to a host in need of the treatment an effective amount of at least one compound as claimed in claim 1.
- 11. A method as claimed in claim 10, wherein the host suffers from impaired lipid metabolism.
- 12. A method as claimed in claim 10, wherein the host suffers from hyperlipidemia.
- 13. A method as claimed in claim 10, wherein the host suffers from an arteriosclerotic symptom.
- 14. A method as claimed in claim 10, wherein the host suffers from insulin resistance.
Priority Claims (2)
| Number |
Date |
Country |
Kind |
| 100 64 402 |
Dec 2000 |
DE |
|
| 101 54 520 |
Nov 2001 |
DE |
|
Parent Case Info
This application claims the benefit of priority under 35 U.S.C. §119(a) to German patent application no. 10064402.3, filed on Dec. 21, 2000, and German patent application no. 10154520.7, filed on Nov. 7, 2001. The contents of both priority documents are incorporated by reference herein.
US Referenced Citations (1)
| Number |
Name |
Date |
Kind |
| 5756470 |
Yumibe et al. |
May 1998 |
A |
Foreign Referenced Citations (5)
| Number |
Date |
Country |
| WO9508532 |
Mar 1995 |
WO |
| WO9535277 |
Dec 1995 |
WO |
| WO9608484 |
Mar 1996 |
WO |
| WO9619450 |
Jun 1996 |
WO |
| WO0001687 |
Jan 2000 |
WO |
Non-Patent Literature Citations (2)
| Entry |
| “Ezetimibe—Hypolipidemic Cholesterol Absorption Inhibitor”, Drugs of the Future, 25(7), pp. 679-685, (2000). |
| Hilgers et al., “Caco-2 Cell Monolayers as a Model for Drug Transport Across the Intestinal Mucosa”, Pharmaceutical Research, 7(9), pp. 902-910, (1990). |
Patent Grant
6498156
