Summary

CLM-103 is a CAR-T cell therapy that recognizes and kills cancer cells expressing IL-13Rα2 protein. IL-13Rα2 is overexpressed in a variety of solid tumors, including malignant glioblastoma but is rarely expressed in normal organs. The antigen-binding domain of CLM-103 is designed to allow intravenous administration by lowering the affinity for IL-13Rα1 expressed in normal cells while binding to the cancer antigen IL-13Rα2. CLM-103 specifically kills cancer cell lines expressing IL-13Rα2, and has shown anticancer efficacy following intravenous administration and then crossing the blood-brain barrier to treat glioblastoma in animals. Phase 1 clinical trial is currently underway on domestic patients with glioblastoma.

Structure and mechanism of action

CLM-103 (YYB-103) uses a modified IL-13 to recognize IL-13Rα2 as its antigen binding domain. It lowers the binding and toxicity to IL-13Rα1 expressed in normal cells through amino acid substitution of IL-13, while maintaining the anticancer activity against IL-13Rα2, therefore achieving anticancer treatment through intravenous administration.

Technical advantage

- CLM-103 is designed to attack only cancer cells without affecting normal cells through CAR structure optimization.

- Since CLM-103 has high selectivity for the cancer antigen IL-13Rα 2, it is safe even during systemic exposure.

- CLM-103 can be delivered to the tumor site, even across the blood-brain barrier, by convenient intravenous administration.

Patent

Research paper

Project	Journal	Year of publication	Title of publication	Link information	Presentation data
CLM-103	Front Immunol.	2021 Nov	Chimeric Antigen Receptor T Cells With Modified Interleukin-13 Preferentially Recognize IL13Rα2 and Suppress Malignant Glioma: A Preclinical Study.

Presentation at academic conference