Antibody-drug conjugates targeting CD19 that internalize into B cells and release a cytotoxic payload to kill malignant cells.
An anti‑CD19 monoclonal antibody binds CD19 on B cells, is internalized, and releases an intracellular cytotoxic payload via linker cleavage, disrupting DNA/mitosis and inducing apoptosis of malignant CD19+ cells (with potential ancillary Fc‑mediated effector activity).
The anti‑CD19 ADC binds CD19, is internalized, and releases a cytotoxic payload after linker cleavage, disrupting DNA/mitosis and inducing apoptosis of CD19+ cells (with possible ancillary Fc‑mediated ADCC/CDC).
Antibody-drug conjugates targeting CD79b (a B-cell receptor component) that internalize and release cytotoxins to kill B-cell lymphomas.
Monoclonal antibody binds CD79b on B-cell receptor, is internalized, and releases its linked cytotoxic payload intracellularly to kill malignant B cells (e.g., via microtubule/DNA damage and apoptosis), with potential Fc-mediated effector contributions.
ADC binds CD79b on B cells, is internalized, and releases a cytotoxic payload that disrupts microtubules/DNA and triggers apoptosis; Fc effector functions (ADCC/CDC) may contribute.
Bispecific antibodies that bind CD20 on B cells and CD3 on T cells to redirect T-cell cytotoxicity against CD20-positive malignant B cells.
Bispecific antibodies that bind CD20 on B cells and CD3 on T cells, bringing T cells into close proximity with CD20+ malignant B cells to form an immunologic synapse and activate T-cell cytotoxicity (perforin/granzyme), leading to MHC-independent killing of target B cells.
CD20×CD3 bispecific antibodies bridge CD20 on B cells to CD3 on T cells, forming an immunologic synapse that activates T-cell cytotoxicity to kill CD20+ cells via perforin/granzyme (MHC-independent).
A gene-modified cellular therapy of gamma-delta (γδ) T cells engineered with a BCMA-targeted chimeric antigen receptor (CAR). Administered as a single infusion to treat relapsed/refractory multiple myeloma by recognizing BCMA (TNFRSF17) on malignant plasma cells and mediating MHC-independent cytotoxicity.
Gamma-delta T cells engineered with a BCMA-targeted CAR bind BCMA (TNFRSF17) on myeloma cells, triggering MHC-independent activation and cytotoxicity (perforin/granzyme release, cytokine secretion, proliferation) to eliminate BCMA+ malignant plasma cells.
BCMA-targeted CAR γδ T cells bind BCMA on target cells, become activated, and directly lyse them via perforin/granzyme–mediated cytotoxicity (MHC-independent), with supportive cytokine-mediated effects.
An anti-HER2 antibody–drug conjugate (RC48) that targets HER2 (ERBB2), internalizes, and releases the cytotoxic payload MMAE to disrupt microtubules and induce apoptosis; may also mediate ADCC and bystander killing.
Anti-HER2 antibody–drug conjugate that binds HER2 (ERBB2) on tumor cells, is internalized, and releases the cytotoxic payload MMAE to inhibit microtubule polymerization, causing G2/M arrest and apoptosis; may also mediate ADCC and bystander killing.
The anti-HER2 ADC binds HER2, is internalized, and releases MMAE that inhibits microtubule polymerization, causing G2/M arrest and apoptosis; Fc-mediated ADCC and bystander killing may also contribute.