[EN] TRICYCLIC COMPOUNDS AS MODULATORS OF TNF-a SYNTHESIS AND AS PDE4 INHIBITORS<br/>[FR] COMPOSÉS TRICYCLIQUES UTILISÉS EN TANT QU'INHIBITEURS DE LA SYNTHÈSE DE TNF-? ET EN TANT QU'INHIBITEURS DE PDE4
申请人:HIGH POINT PHARMACEUTICALS LLC
公开号:WO2009094528A1
公开(公告)日:2009-07-30
The present invention relates to chemical compounds of Formula (I) are as herein defined, pharmaceutical compositions, and methods of use in the treatment of conditions or disorders mediated by TNF-alpha or by PDE4, including but not limited to rheumatoid arthritis.
Tricyclic Compounds As Modulators of TNF-alpha Synthesis
申请人:Mjalli Adnan M. M.
公开号:US20100190808A1
公开(公告)日:2010-07-29
The present invention relates to chemical compounds of Formula (I) are as herein defined, pharmaceutical compositions, and methods of use in the treatment of conditions or disorders mediated by TNF-alpha or by PDE4, including but not limited to rheumatoid arthritis.
Tricyclic Compounds as Modulators of TNF-alpha Synthesis and as PDE4 Inhibitors
申请人:Mjalli Adnan M.M.
公开号:US20110160234A1
公开(公告)日:2011-06-30
The present invention relates to chemical compounds of Formula (I) are as herein defined, pharmaceutical compositions, and methods of use in the treatment of conditions or disorders mediated by TNF-α or by PDE4, including but not limited to rheumatoid arthritis.
Tricyclic compounds as modulators of TNF-α synthesis
申请人:High Point Pharmaceuticals, LLC
公开号:US07964608B2
公开(公告)日:2011-06-21
The present invention relates to chemical compounds of Formula (I) are as herein defined, pharmaceutical compositions, and methods of use in the treatment of conditions or disorders mediated by TNF-alpha or by PDE4, including but not limited to rheumatoid arthritis.
Tricyclic compounds as modulators of TNF-α synthesis and as PDE4 inhibitors
申请人:High Point Pharmaceuticals, LLC
公开号:US08329715B2
公开(公告)日:2012-12-11
The present invention relates to chemical compounds of Formula (I) are as herein defined, pharmaceutical compositions, and methods of use in the treatment of conditions or disorders mediated by TNF-α or by PDE4, including but not limited to rheumatoid arthritis.