FcRn-based therapeutics for the treatment of auto-immune disorders
US6992234B2 · kind B2 · utility
Assignee
Inventor
Key dates
| Filing date | Nov 6, 2001 |
| Grant date | Jan 31, 2006 |
| Priority date | — |
| Expiry date | Aug 24, 2022 |
Classification
- Technology area (CPC A)Human Necessities
- CPC primaryA61K2039/505
- WIPO fieldPharmaceuticals
- WIPO sectorChemistry
Abstract
Disclosed is a transgenic knockout mouse whose genome comprises a homozygous disruption in its endogenous FcRn gene. The homozygous FcRn disruption prevents the expression of a functional FcRn protein, resulting in a transgenic knockout mouse in which exogenously administered IgG1 exhibits a substantially shorter half-life, as compared to the half-life of exogenously administered IgG1 in a wild-type mouse. The transgenic knockout mouse with a homozygous FcRn disruption is also unable to absorb maternal IgG in the prenatal or neonatal stage of development. Also disclosed is a transgenic knockout mouse comprising a homozygous FcRn disruption and a human FcRn transgenic. The transgenic addition of human FcRn results in a substantial increase in the half-life of exogenously administered human IgG1. Methods of using the transgenic knockout mouse, and cells derived from them, are also disclosed.
Source: USPTO / EPO open patent data. Objective bibliographic and citation counts.