Also known as RC48, an antibody–drug conjugate targeting HER2 (ERBB2) that delivers the microtubule inhibitor MMAE via a cleavable linker, leading to internalization, microtubule disruption, apoptosis, and bystander killing.
Anti-HER2 (ERBB2) antibody–drug conjugate that binds HER2 on tumor cells, is internalized, and via a cleavable linker releases monomethyl auristatin E (MMAE). MMAE binds tubulin and inhibits microtubule polymerization, inducing G2/M arrest and apoptosis, with potential bystander killing due to the membrane-permeable payload.
NO
INDIRECT
The ADC binds HER2 (not tubulin) on tumor cells, is internalized, and releases MMAE, which binds beta-tubulin at the vinca site to disrupt microtubules, causing G2/M arrest and apoptosis; bystander killing may occur, but tubulin expression itself is not the selection target.
ADCC-enhanced monoclonal antibody targeting GPRC5D; Fc engineering increases binding to Fc gamma receptors (e.g., CD16) to activate NK cells and mediate antibody-dependent cellular cytotoxicity against malignant plasma cells.
Fc-engineered monoclonal antibody that binds GPRC5D on malignant plasma cells and has increased affinity for Fcγ receptors (e.g., CD16) to more effectively recruit NK cells (and other FcγR+ effector cells), triggering antibody-dependent cellular cytotoxicity (and potentially ADCP/CDC) to kill myeloma cells.
YES
DIRECT
The antibody binds GPRC5D on myeloma cells and its Fc engages Fc gamma receptors (e.g., CD16) on NK cells to trigger ADCC (perforin/granzyme), with possible ADCP/CDC.
Autologous, gene-modified T lymphocytes expressing a chimeric antigen receptor targeting CD276 (B7-H3) for recurrent/progressive glioblastoma; intracranial (Ommaya) delivery with weekly dosing in a 3+3 escalation (5×10^6 then 1×10^7 cells). Redirects T cells independent of native TCR, activating CAR signaling (CD3ζ with costimulation), cytokine release, and perforin/granzyme-mediated cytotoxicity against CD276-positive tumor and vasculature.
Autologous T lymphocytes engineered to express a CD276 (B7-H3)-specific chimeric antigen receptor. CAR binding to CD276 on tumor cells and tumor vasculature activates CD3ζ and costimulatory signaling, driving T-cell activation, cytokine release, and perforin/granzyme-mediated cytotoxic killing independent of the native TCR.
YES
DIRECT
CAR-T cells recognize CD276 on target cells, triggering CD3ζ/costimulatory signaling and T-cell cytotoxicity via perforin/granzyme release (with cytokine-mediated effects).
ADCC-enhanced monoclonal antibody targeting GPRC5D; Fc engineering increases binding to Fc gamma receptors (e.g., CD16) to activate NK cells and mediate antibody-dependent cellular cytotoxicity against malignant plasma cells.
Fc-engineered monoclonal antibody that binds GPRC5D on malignant plasma cells and has increased affinity for Fcγ receptors (e.g., CD16) to more effectively recruit NK cells (and other FcγR+ effector cells), triggering antibody-dependent cellular cytotoxicity (and potentially ADCP/CDC) to kill myeloma cells.
NO
INDIRECT
SAR446523 binds GPRC5D on myeloma cells; its Fc engages CD16a on NK cells to trigger ADCC that kills GPRC5D+ tumor cells. CD16a+ cells are effectors and are not targeted for killing.
A T cell–engaging bispecific antibody immunotherapy that binds Claudin 18.2 on tumor cells and CD3 on T cells to redirect and activate endogenous T cells, inducing cytotoxic killing of tumor cells; administered intravenously or subcutaneously.
Affinity-optimized bispecific antibody that binds CLDN18.2 on tumor cells (bivalent, high affinity) and CD3 on T cells (monovalent, low affinity), crosslinking tumor cells and T cells to activate and expand cytotoxic T lymphocytes, triggering TCR signaling, immune synapse formation, cytokine release, and lysis of CLDN18.2-positive tumor cells with potential bystander killing.
YES
DIRECT
Bispecific T‑cell engager binds CLDN18.2 on tumor cells and CD3 on T cells, crosslinking to activate CTLs and form an immune synapse, leading to perforin/granzyme-mediated lysis of CLDN18.2+ cells (with potential bystander killing).