Seminars
May 12, 2026
Engineering Chimeric Bifunctional Antibodies for Membrane Protein Degradation
Speaker: Dr. Dingpeng Zhang
Postdoctoral Research Fellow, Department of Pathology, Beth Israel Deaconess Medical Center, Harvard Medical School
School of Biomedical Sciences cordially invites you to join the following seminar:
Date: 12 May 2026 (Tuesday)
Time: 2:00 pm – 3:00 pm
Venue: Seminar Room 1, G/F, Laboratory Block, 21 Sassoon Road
Host: Professor Clive Chung
Biography
Dingpeng Zhang received his B.S. and M.S. degrees in Pharmaceutical Engineering from Jilin University and a Ph.D. in Chemical Biology from Nanyang Technological University. He is currently a postdoctoral scholar at Beth Israel Deaconess Medical Center, Harvard Medical School. His research program bridges Chemical Biology and Pharmaceutical Sciences, with a focus on programmable protein degradation and stabilization strategies. During his postdoctoral training, he developed several first-in-class therapeutic platforms—including Transferrin Receptor–targeted Chimeras (TransTACs), degrader–antibody drug conjugates (ADCs/DDCs), folate-directed lysosome-targeting chimeras (FolTACs), and deubiquitinase-targeting chimeras (DUBTACs)—that offer novel strategies for inhibiting cancer growth and activating immune cells. These innovations have been published in top-tier journals such as Nature, Nature Communications, and JACS, as well as covered in multiple patents.
Abstract
Cancer cells require high levels of iron for rapid proliferation, leading to significant upregulation of cell-surface transferrin receptor 1 (TfR1), which mediates iron uptake by binding to the iron-carrying protein transferrin1. Leveraging this phenomenon and the fast endocytosis rate of TfR1, we developed transferrin receptor targeting chimeras (TransTACs), a heterobispecific antibody modality for membrane protein degradation. TransTACs are engineered to drive rapid co-internalization of a target protein of interest and TfR1 from the cell surface, and to enable target protein entry into the lysosomal degradation pathway. We show that TransTACs can efficiently degrade a diverse range of single-pass, multi-pass, native or synthetic membrane proteins, including Epidermal Growth Factor Receptor (EGFR), programmed cell death 1 ligand 1 (PD-L1), cluster of differentiation 20 (CD20) and chimeric antigen receptor (CAR). TransTACs enabled the reversible control of human primary chimeric antigen receptor T cells and the targeting of drug-resistant epidermal growth factor receptor-driven lung cancer with the exon 19 deletion/T790M/C797S mutations. TransTACs represent a promising new family of bifunctional antibodies for precise manipulation of membrane proteins and targeted cancer therapy.
All are welcome.
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