BASEL, Switzerland & CAMBRIDGE, Mass.--(BUSINESS WIRE)--Cimeio Therapeutics, a biotechnology company leading the field of epitope shielding, is presenting data for its CD52 program during this week’s Annual Meeting of the American Society of Cell & Gene Therapy (ASGCT) in Baltimore. The abstract is titled “Molecular Shielding of CD52 Retains Expression, Anti-Phagocytic Don’t Eat Me Function and Protects from Alemtuzumab-Mediated Depletion.”
The study is the first showing that T cells expressing an engineered CD52 can be effectively shielded from Alemtuzumab-mediated depletion, while maintaining the general features of this receptor. Cimeio's research team also showed for the first time that CD52 mediates an anti-phagocytotic ‘Don’t Eat Me’ signal, which is retained by the engineering. This program can serve as the basis for a novel approach to treating patients with T cell malignancies, non-genotoxic conditioning, and aiding in improving the persistence of allogeneic CAR T cells.
“Exhaustive screening as well as comprehensive expression, glycan and functional analyses allowed us to identify a base editable point mutation that protected T cells from Alemtuzumab, while allowing CD52 to maintain its cell surface expression, processing and function,” said Stefanie Urlinger, Ph.D., Chief Scientific Officer at Cimeio. “We are excited to explore the full potential of our engineered CD52 receptor in the future. This can represent a viable alternative to CD52 knock-out on allogeneic CAR T cells, mediating resistance to lymphodepletion using Alemtuzumab and perhaps also contributing to a prolonged in vivo persistence.”
Dr. Urlinger will present the findings at 5:30 PM ET on Friday, May 10, as poster number 1,778.
About Cimeio
Cimeio is the leader of the field of epitope shielding and is developing a portfolio of Shielded-Cell & Immunotherapy Pairs™ (SCIP), novel immunotherapies which have the potential to transform treatment of hematologic diseases. Cimeio develops state-of-the-art immunotherapies, along with paired, modified variants of naturally occurring cell surface proteins in HSCs. These novel epitope edited variants maintain their function but are resistant to depletion when targeted by the paired immunotherapy which has high affinity for the wild-type version of these proteins. These immunotherapies have significant therapeutic potential, which Cimeio is using to develop curative treatments for patients with hematologic malignancies, autoimmune disorders, and genetic diseases. Shielded Cell and Immunotherapy Pairs and SCIP are trademarks of Cimeio Therapeutics, Inc. For more information, please visit www.cimeio.com.
