Uncovering the anti-cancer mechanisms of Immuno-Oncology

GNTbm-38, through its unique epigenetic regulatory and immune activation mechanisms, can be used in combination with a specific TKI to restructure the TME, attracting CTL infiltration into the TME for selectively attacking the tumor, and inhibiting the attraction of immunosuppressive cells to the TME. This generates a powerful tumor immune cytotoxic effect on cancer cells and can produce lasting immune memory, which is beneficial for sustained anti-cancer effects without recurrence. Many solid tumors classified as 'cold tumors' are suitable for this approach. On the other hand, the anti-PD1/VEGF bispecific antibody shows superior therapeutic benefits compared to anti-PD-1 monoclonal antibodies and has been recognized as an essential component in future cancer immunotherapy. Therefore, the combination of GNTbm-38 with anti-PD-1/VEGF bispecific antibody will provide excellent cancer immunotherapy benefits, primarily through the epigenetic regulation and immune activation mechanisms of GNTbm-38. When combined with anti-VEGF antibody, it can effectively remodel the TME, turning 'cold tumors' into 'hot tumors', while anti-PD-1 antibody further activate CTL's tumor-attacking activity. This cooperative action of three different drug mechanisms not only remodels the TME but also activates CTL for persistent tumor attack, significantly enhancing the effects of cancer immunotherapy.

Further divide the drug combinations into: