Developing anti-LAG-3 therapeutic monoclonal antibodies for colorectal cancer immunotherapy is the goal of the anti-Lag program.

Justification for the program:

Despite significant advancements in the treatment of advanced cancers, most individuals with a variety of tumor types do not react to CTLA4 and PD1-PDL1. Therefore, in order to identify alternative treatment targets, the attention must be shifted to a thorough investigation of the tumor microenvironment.

Immune homeostasis is maintained by lymphocyte activating gene-3 (LAG3) (CD223), which prevents T cell activation and cytokine release. LAG3 expression is sustained in the tumor microenvironment as a result of ongoing antigen exposure.

Research has demonstrated the noteworthy synergistic effects of LAG3 and PD1 in a range of clinical contexts, underscoring the possible specialization of LAG3.

In light of the foregoing, LAG3 represents a viable immunological checkpoint for therapeutic use.