Next-IO™ NK Cell related Therapeutics

By leveraging the NKG2D pathway, this program engineers fusion proteins to activate both NK and T cell responses. Specialized constructs, such as cytokine fusions and bispecific engagers, are provided for cancer research models.

To reverse tumor-induced immunosuppression, we develop non-blocking neutralizing antibodies against soluble MIC (sMIC). Revamping both innate and adaptive immune responses allows these therapeutics to target metastatic tumors.

Targeting the overexpressed CD48 ligand found in multiple myeloma, this program creates therapeutic antibodies that induce immune-mediated cytotoxicity. These candidates effectively inhibit tumor cell growth while preserving healthy progenitor cells.

NK and CD8+ T cell cytotoxicity can be restored in research models by developing antibodies that block the 2B4 (CD244) inhibitory receptor. This blockade disrupts 2B4/CD48 interactions to enable efficient cancer cell attacks.

Our researchers develop antibodies to block HLA-G interactions with inhibitory receptors like KIR2DL4. Neutralizing HLA-G suppresses tumor immune evasion and restores NK cell cytotoxicity within various research models.

Restoring NK cell cytotoxicity is the primary goal of this therapeutic antibody program targeting the KIR2DL4 receptor. These candidates modulate inhibitory signals to enhance innate antitumor responses and overcome tumor evasion.

Blocking the KIR2DL1-3 inhibitory receptors on NK cells allows for enhanced cytotoxicity against tumor cells. By disrupting MHC-I/KIR interactions, these antibodies restore immune function in research models.

We engineer antibodies to target the CD94/NKG2A inhibitory receptor and block its binding to HLA-E. This neutralization effectively reverses immunosuppression by restoring NK cell cytokine production.

To prevent tumor immune escape, this program develops antibodies that neutralize the Poliovirus Receptor (PVR/CD155). This action blocks inhibitory interactions with CD96, thereby restoring NK cell anti-tumor cytotoxicity.

Cytokine production is restored and tumor metastasis is prevented through the development of antibodies against the CD96 (TACTILE) receptor. This approach neutralizes the inhibitory interaction between CD96 and CD155/PVR.

Monoclonal antibodies with optimized Fc regions are developed here to maximize CD16 (FcγRIIIa) engagement. Such optimization triggers potent ADCC and tumor apoptosis in diverse oncology research settings.

Neutralizing the LILRB1 inhibitory receptor blocks its interaction with MHC-I/HLA-G, thereby enhancing innate and adaptive immunity. These antibodies restore the cytotoxic potential of NK and T cells.

This initiative develops therapeutic antibodies to block the KLRG1 inhibitory receptor from binding with cadherin ligands. Effector functions are restored and antitumor efficacy is enhanced through this specific blockade.

Cadherin-targeted antibodies are developed to disrupt tumor cell adhesion and inhibit metastasis. These candidates also block inhibitory signaling to restore NK cell effector functions in research models.

By blocking the interaction between LLT1 (CLEC2D) and NKRP1A, these therapeutic antibodies enhance NK cell-mediated cytotoxicity. The program aims to reverse immune evasion across several cancer models.

Antitumor efficacy against breast and prostate cancer models is enhanced through antibodies targeting the NKRP1A (CD161) receptor. Neutralizing this receptor restores vital NK cell cytotoxicity.

Innovative antibody-sialidase conjugates desialylate tumor cells to disrupt Siglec-mediated inhibitory signaling. Reactivating NK cell cytotoxicity reverses glycan-mediated evasion in solid tumor research.

Neutralizing Nectin-2 (CD112) suppresses tumor progression by disrupting its inhibitory binding with PVRIG and TIGIT. This restore-and-restrain strategy maximizes NK cell-mediated cytotoxicity.