Amelioration of collagen-induced arthritis in mice by a novel phosphodiesterase 7 and 4 dual inhibitor, YM-393059

Eur J Pharmacol. 2007 Mar 22;559(2-3):219-26. doi: 10.1016/j.ejphar.2006.11.079. Epub 2006 Dec 12.

Abstract

YM-393059 is a novel phosphodiesterase (PDE) 7 and PDE4 dual inhibitor that inhibits PDE7A with high potency (IC50=14 nM) and PDE4 with moderate potency (IC50=630 nM). It inhibits lipopolysaccharide (LPS)-induced tumor necrosis factor-alpha production in mice with an ED50 value of 2.1 mg/kg [Yamamoto, S., Sugahara, S., Naito, R., Ichikawa, A., Ikeda, K., Yamada, T., Shimizu, Y., 2006. The effects of a novel phosphodiesterase 7A and -4 dual inhibitor, YM-393059, on T-cell-related cytokine production in vitro and in vivo. Eur. J. Pharmacol. 541, 106-114.]. In this study, we investigated the therapeutic potential of YM-393059 for the treatment of rheumatoid arthritis in several animal models. YM-393059 was found to inhibit LPS-induced interleukin (IL)-1beta production in mice with an ED50 value of 16.6 mg/kg, but it had only a slight effect on IL-6 production. YM-393059 and cyclosporine significantly suppressed arthritis development at doses of 30-100 mg/kg and 20 mg/kg, respectively, in the mice collagen-induced arthritis model. YM-393059 (100 mg/kg) significantly inhibited increases in the serum immunoglobulin G level that occurred in response to autoantigenic collagen in arthritic mice, whereas cyclosporine (20 mg/kg) did not. In contrast, cyclosporine completely suppressed the acute rejection of cardiac allografts in rats, whereas YM-393059 did not, even at a dose of 100 mg/kg. YM-393059 potently inhibited proinflammatory cytokine production and selectively suppressed the response to the autoantigen without affecting the response to alloantigens. These results suggest that YM-393059 is an attractive compound for the treatment of autoimmune disorders such as rheumatoid arthritis.

Publication types

  • Comparative Study

MeSH terms

  • 3',5'-Cyclic-AMP Phosphodiesterases / antagonists & inhibitors*
  • 3',5'-Cyclic-AMP Phosphodiesterases / metabolism
  • Animals
  • Antibody Formation / drug effects
  • Antirheumatic Agents / pharmacology*
  • Antirheumatic Agents / therapeutic use
  • Arthritis, Experimental / enzymology
  • Arthritis, Experimental / immunology
  • Arthritis, Experimental / prevention & control*
  • Arthritis, Rheumatoid / enzymology
  • Arthritis, Rheumatoid / immunology
  • Arthritis, Rheumatoid / prevention & control*
  • Cyclic Nucleotide Phosphodiesterases, Type 4
  • Cyclic Nucleotide Phosphodiesterases, Type 7
  • Cyclosporine / pharmacology
  • Dose-Response Relationship, Drug
  • Fumarates / pharmacology*
  • Fumarates / therapeutic use
  • Graft Survival / drug effects
  • Heart Transplantation
  • Immunoglobulin G / blood
  • Immunosuppressive Agents / pharmacology
  • Indoles / pharmacology*
  • Indoles / therapeutic use
  • Interleukin-1beta / biosynthesis
  • Interleukin-6 / biosynthesis
  • Male
  • Mice
  • Mice, Inbred BALB C
  • Mice, Inbred DBA
  • Phosphodiesterase Inhibitors / pharmacology*
  • Phosphodiesterase Inhibitors / therapeutic use
  • Rats
  • Rats, Inbred Lew
  • Sulfonamides / pharmacology*
  • Sulfonamides / therapeutic use
  • Time Factors
  • Transplantation, Homologous

Substances

  • Antirheumatic Agents
  • Fumarates
  • Immunoglobulin G
  • Immunosuppressive Agents
  • Indoles
  • Interleukin-1beta
  • Interleukin-6
  • N-(4,6-dimethylpyrimidin-2-yl)-4-(2-(4-methoxy-3-methylphenyl)-5-(4-methylpiperazin-1-yl)-4,5,6,7-tetrahydro-1H-indol-1-yl)benzenesulfonamide difumarate
  • Phosphodiesterase Inhibitors
  • Sulfonamides
  • Cyclosporine
  • 3',5'-Cyclic-AMP Phosphodiesterases
  • Cyclic Nucleotide Phosphodiesterases, Type 4
  • Cyclic Nucleotide Phosphodiesterases, Type 7
  • Pde7a protein, mouse
  • Pde7a protein, rat