Chimeric IgG1 monoclonal antibody that binds and neutralizes TNF-alpha (soluble and transmembrane) to reduce inflammatory signaling.
Chimeric IgG1 monoclonal antibody that binds both soluble and transmembrane TNF-α, neutralizing TNF and preventing TNFR1/2 activation. This suppresses downstream NF-κB–driven inflammatory signaling and cytokine production; may also mediate Fc-dependent effector functions (ADCC/CDC) against TNF-expressing cells.
Binds transmembrane TNF-alpha and, via its IgG1 Fc, triggers ADCC and complement-mediated lysis (CDC); can also induce apoptosis via reverse signaling through tmTNF.
An autologous NKG2D-based CAR T-cell therapy in which patient T cells are gene-engineered to express a chimeric antigen receptor using the NKG2D receptor ectodomain fused to intracellular activation/costimulatory domains (e.g., CD3ζ). The cells target stress-induced NKG2D ligands (MICA, MICB, ULBP1–6) on tumor cells to mediate cytotoxicity and cytokine release.
Autologous T cells are engineered to express an NKG2D-based CAR (NKG2D ectodomain fused to 4-1BB and CD3ζ signaling domains) that recognizes stress-induced NKG2D ligands (MICA, MICB, ULBP1–6) on tumors, activating T cells to release cytokines and mediate perforin/granzyme-dependent cytotoxicity against NKG2DL-positive cancer cells.
NKG2D CAR T cells bind MICB on target cells, activate, and induce perforin/granzyme-mediated cytolysis (with cytokine release).
IV humanized monoclonal antibody targeting HER2 (ErbB2); inhibits signaling and mediates ADCC.
Humanized anti-HER2 (ErbB2) IgG1 monoclonal antibody that binds HER2 on tumor cells, inhibits receptor signaling and dimerization, and triggers antibody-dependent cell-mediated cytotoxicity (ADCC) against HER2-overexpressing cells.
Binds HER2 on tumor cells and recruits FcγR-expressing immune effectors (e.g., NK cells) to induce antibody-dependent cell-mediated cytotoxicity (ADCC); may also activate complement. Signaling blockade is non-cytolytic.
Anti-HER2 antibody–drug conjugate delivering the microtubule inhibitor DM1 to HER2-expressing cells.
Trastuzumab (anti‑HER2 mAb) conjugated to DM1, a maytansinoid microtubule inhibitor. After binding HER2 on tumor cells, the complex is internalized and DM1 is released intracellularly to disrupt microtubules, causing cell-cycle arrest and apoptosis; trastuzumab also inhibits HER2 signaling and can mediate ADCC.
Binds HER2, is internalized, and releases the DM1 payload inside the cell to disrupt microtubules, causing mitotic arrest and apoptosis; Fc can also mediate ADCC.
An autologous NKG2D-based CAR T-cell therapy in which patient T cells are gene-engineered to express a chimeric antigen receptor using the NKG2D receptor ectodomain fused to intracellular activation/costimulatory domains (e.g., CD3ζ). The cells target stress-induced NKG2D ligands (MICA, MICB, ULBP1–6) on tumor cells to mediate cytotoxicity and cytokine release.
Autologous T cells are engineered to express an NKG2D-based CAR (NKG2D ectodomain fused to 4-1BB and CD3ζ signaling domains) that recognizes stress-induced NKG2D ligands (MICA, MICB, ULBP1–6) on tumors, activating T cells to release cytokines and mediate perforin/granzyme-dependent cytotoxicity against NKG2DL-positive cancer cells.
NKG2D-based CAR T cells recognize ULBP1 on target cells, activate, and induce perforin/granzyme-mediated cytolysis with cytokine release.