Checkpoint inhibitors do not kill cancers. They remove checkpoints which prevent activated T cells from doing this. Checkpoints put a brake on normal immunologic mechanisms to eliminate cancers.
Waning of PD1 anticancer effect can be due to T cell exhaustion which can be overcome by our fusion protein, eftilagimod.
Eftilagimod allows reprogramming cellular immunity adapting to changing antigen environments. This is active immunotherapy c/w CAR T cell passive immunotherapies.
This paper points out that PD1 monotherapy may already be outdated and there is a need to include eftilagimod or similar therapies for sustained improvements.
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