Validation experiment designed to validate causal mechanisms targeting IGHG1 in B6.Cg-Fcgrttm1Dcr Tg(FCGRT)32Dcr transgenic mice. Primary outcome: Production of human IgG1 Fc-mouse IgG Fab2 chimeric antibodies
This experiment involved using CRISPR/Cas9-mediated homology-directed repair to replace the mouse immunoglobulin heavy constant gamma 1 (IGHG1) Fc domain with the human IGHG1 Fc domain in hFCGRT transgenic mice (Tg32 strain). The goal was to create mice that produce human IgG1 Fc-mouse IgG Fab2 chimeric antibodies at physiologically relevant levels to better model human competitive conditions for IgG-based biologics. The engineered mice were designed to provide endogenous human IgG competition that more accurately reflects human physiology, addressing a recognized limitation of existing FcRn-humanized mouse models that lack endogenous human IgG.
CRISPR/Cas9-mediated homology-directed repair to replace mouse IGHG1 Fc domain with human IGHG1 Fc domain in hFCGRT transgenic mice
Mice producing physiologically relevant levels of human IgG1 Fc-containing chimeric antibodies that can compete with administered humanized mAbs
Production of chimeric IgG1 at physiologically relevant levels and demonstration of competitive effects on humanized mAb pharmacokinetics
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