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During the congress, E-Posters will be accessible to all participants on the congress website 24/7, as well as in the E-poster stations in the congress center.
Preparing your E-Poster
Please review the E-Poster format requirements carefully when preparing your E-Poster. Should your E-Poster not meet the mentioned requirements, it may not be displayed as described above.
E-Poster Submission Deadline
Please prepare and upload your E-Poster no later than March 14, 2026 11.59PM CET. After this date, you will no longer be able to prepare and upload your E-poster and it will not be displayed and accessible on the congress website.
Please follow the instructions below to input your abstract title.
Abstract titles should be brief and reflect the content of the abstract.
IgA nephropathy (IgAN), the most common primary glomerulonephritis worldwide, is characterized by glomerular mesangial deposition of IgA1 immune complexes. Galactose-deficient IgA1 (Gd-IgA1) is a key pathogenic driver of the disease. Reducing its levels represents a promising therapeutic strategy.
Here, we leverage the rapid endocytic recycling of transferrin receptor 1 (TfR1) to design a bispecific antibody that co-binding Gd-IgA1 and TfR1. This approach aims to redirect Gd-IgA1 into the lysosomal degradation pathway via TfR1-mediated internalization.
We isolated an anti-Gd-IgA1 antibody using phage display and engineered it into a TfR1-targeting bispecific antibody. Biolayer interferometry confirmed dual binding specificity. Cellular assays demonstrated efficient internalization of the bispecific antibody, with colocalization observed in early, late, and recycling endosomes marked by Rab5, Rab7, and Rab11.
Our study establishes TfR1 as an effective membrane protein for targeted degradation of pathogenic Gd-IgA1 and highlights the therapeutic potential of this bispecific antibody platform for the treatment of IgAN.