Chugai Seiyaku Kabushiki Kaisha

University of Pennsylvania

Other

Yoshinobu Higuchi

Tatsuo Tanaka

Hidetomo Kitamura

Masahiro Iwamoto

Maurizio Pacifici

Yuki Iwayanagi

Keiko Hirokawa

Ryosuke Mihara

Akihisa Kaneko

Joel Rosenbloom

Hiroaki Matsushita

Yumi Yamamoto

Tomohisa Saito

Tomoyuki Igawa

Hiroyuki Tsunoda

Atsuhiko Maeda

Tatsuhiko Tachibana

Hirotake Shiraiwa

Tetsuo Kojima

Shinya Ishii

Mika Sakurai

Keiko Kasutani

Masakazu Hasegawa

In a non-limiting embodiment, there is provided a pharmaceutical composition for prevention and/or treatment of atopic dermatitis comprising an IL-31 antagonist as an active ingredient, wherein the IL-31 antagonist is repeatedly administered in equal amounts at the same dosing interval to a subject with or potentially with atopic dermatitis, at 0.1 to 1000 mg/body/1 day to 12 weeks, preferably at 0.1 to 1000 mg/body/2 weeks, 0.1 to 1000 mg/body/4 weeks, or 0.1 to 1000 mg/body/8 weeks.

Pharmaceutical composition for prevention and/or treatment of atopic dermatitis comprising IL-31 antagonist as active ingredient

The present invention provides pharmaceutical compositions comprising second-generation molecules that are superior than TOCILIZUMAB, by altering the amino acid sequences of the variable and constant regions of TOCILIZUMAB, which is a humanized anti-IL-6 receptor IgG1 antibody, to enhance the antigen-neutralizing ability and increase the pharmacokinetics, so that the therapeutic effect is exerted with a less frequency of administration, and the immunogenicity, safety and physicochemical properties (stability and homogeneity) are improved. The present invention also provides methods for producing these pharmaceutical compositions. The present inventors have successfully generated second-generation molecules that are superior to TOCILIZUMAB by appropriately combining amino acid sequence alterations in the CDR domains, variable regions, and constant regions.

Methods of reducing IL-6 activity for disease treatment

Antibody molecules that bind to IL-6 receptor

The present inventors isolated clone BM095 from a human antibody phage library, which had a strong growth inhibitory activity in the IL-31-dependent Ba/F3 cell growth assay system. When administered to pruritus model mice, the anti-mouse NR10 neutralizing antibody exhibited a marked symptom-suppressing effect. Thus, it was revealed that anti-NR10 neutralizing antibodies are useful as therapeutic agents for pruritus.

Method for treating pruritus comprising administering an NR10 antagonist

This invention provides cell-calcification inhibitory proteins as well as genes encoding the proteins. Based on the discovery of a novel isoform gene of the c-erg gene (herein referred to as 'C-11 gene') which is an erg gene derived from chickens, the nucleotide sequence of the gene has been determined, and then the expression of a protein encoded by such gene (herein referred to as 'C-11 protein') has been confirmed. Further, it has been discovered that when the c-erg or C-11 gene is introduced into osteoblasts, the calcification of the cells is inhibited.

Cell calcification suppressing proteins, and genes of the proteins

This invention provides cell-calcification inhibitory proteins as well as genes encoding the proteins. Based on the discovery of a novel isoform gene of the c-erg gene (herein referred to as &ldquo;C-11 gene&rdquo;) which is an erg gene derived from chickens, the nucleotide sequence of the gene has been determined, and then the expression of a protein encoded by such gene (herein referred to as &ldquo;C-11 protein&rdquo;) has been confirmed. Further, it has been discovered that when the c-erg or C-11 gene is introduced into osteoblasts, the calcification of the cells is inhibited.

Cell calcification supressing proteins, and genes of the proteins

Growing community of inventors

Shizuoka, Japan

Yoshinobu Higuchi