Transgenic mouse expressing human FcRn protein
US7358416B2 · kind B2 · utility
Assignee
Inventor
Key dates
| Filing date | Sep 27, 2005 |
| Grant date | Apr 15, 2008 |
| Priority date | — |
| Expiry date | Mar 16, 2026 |
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 RcRn 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 RcRn 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 transgene. 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.