TNF-A and TWEAK dual antagonist for the prophylaxis and treatment of autoimmune diseases
US8916525B2 · kind B2 · utility
Assignees
Inventors
Key dates
| Filing date | Mar 18, 2011 |
| Grant date | Dec 23, 2014 |
| Priority date | — |
| Expiry date | Mar 18, 2031 |
Classification
- Technology area (CPC C)Chemistry; Metallurgy
- CPC primaryC07K2319/32
- WIPO fieldPharmaceuticals
- WIPO sectorChemistry
Abstract
The present invention relates to TNFR2-TWEAKR fusion protein, more precisely to TNFR2-TWEAKR fusion protein acting as a double-antagonist to TNF-α and TWEAK, known as major causes of autoimmune arthritis which is one of autoimmune diseases. When the composition comprising TNFR2-TWEAKR fusion protein was treated to Th17 cells, the secretion of the inflammatory cytokine IL-17 was reduced but the secretion of the anti-inflammatory cytokine IL-10 generated in Treg cells was increased. Such effect of TNFR2-TWEAKR fusion protein was far greater than that of a single protein such as TNFR2-Fc or TWEAK-Fc. The TNFR2-TWEAKR fusion protein of the present invention has not only excellent treatment effect on arthritis in CIA mouse model not also excellent treatment effect on autoimmune rheumatoid arthritis by increasing the expression of Treg, the immune suppressive cells. Therefore, the TNFR2-TWEAKR fusion protein of the present invention can be effectively used as an active ingredient for the composition for the prevention and treatment of autoimmune disease.
Source: USPTO / EPO open patent data. Objective bibliographic and citation counts.