DAF-CR1 Hybrid Protein 1 (3I3)
- 詳細技術說明
- Provides polypeptides that are potent inhibitors of inflammation and may be used to treat or slow progression of inflammation-related diseases such as inflammatory bowel syndrome (IBS), myasthenia gra
- *Abstract
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Provides polypeptides that are potent inhibitors of inflammation and may be used to treat or slow progression of inflammation-related diseases such as inflammatory bowel syndrome (IBS), myasthenia gravis, or rheumatoid arthritis. Decay Accelerating Factor (DAF, CD55) is a membrane-associated regulatory protein that protects self cells from activation of autologous complement on their surfaces. DAF acts by rapidly dissociating C3 and C5 convertases, the central enzymes of the cascade. DAF possesses the most potent decay accelerating activity of the proteins associated with complement regulation, and acts on both the classical pathway (C4b2a and C4b2a3b) and alternative pathway (C3bBb and C3bBbC3b) enzymes. DAF, however, does not have cofactor function. The technology discloses a fusion protein that combines two complement inhibitory proteins, Decay Accelerating Factor (DAF) and Complement Receptor Type 1 (CR1). Each of these proteins acts to inhibit complement at different points of the activation pathway. While DAF only accelerates the decay or disassociation of the amplifying enzymes of the pathway, CR1 also inactivates components of those enzymes. Although CR1 does have decay accelerating capabilities, DAF is more efficient at performing this function. Therefore, combining the activities of the two proteins into one provides a potent complement inhibitory protein as demonstrated in two experimental models. Furthermore, the two proteins each exist as membrane bound proteins whereas the invention is a soluble protein, which may further increase its potency. The recombinant protein may be used to treat any complement-mediated disease. Published as US 2008-0188404 A1, 7-Aug-2008.
- 國家/地區
- 美國
