HER2-targeted antibody–drug conjugate that, after binding HER2, is internalized and releases MMAE to disrupt microtubules, causing mitotic arrest and apoptosis; can also mediate ADCC.
HER2-targeted monoclonal antibody linked to the cytotoxic payload MMAE. After binding HER2 on tumor cells, the ADC is internalized and the linker is cleaved to release MMAE, which disrupts microtubules to induce G2/M arrest and apoptosis; the antibody Fc can also mediate ADCC.
The HER2-binding ADC is internalized after binding HER2; linker cleavage releases MMAE inside the cell, disrupting microtubules to cause G2/M arrest and apoptosis. The antibody Fc can also mediate ADCC against HER2+ cells.
CD79b-targeted antibody–drug conjugate that delivers monomethyl auristatin E (MMAE) to B cells, disrupting microtubules and inducing apoptosis.
Monoclonal antibody targets CD79b on B cells, is internalized, and releases the cytotoxin MMAE via a protease-cleavable linker; MMAE inhibits tubulin polymerization, disrupting microtubules, causing G2/M arrest and apoptosis of malignant B cells.
Antibody-drug conjugate binds CD79b, is internalized, and releases MMAE after linker cleavage; MMAE inhibits tubulin polymerization, causing G2/M arrest and apoptosis of CD79b+ cells.
Chimeric anti-CD20 monoclonal antibody that depletes B cells via complement-dependent cytotoxicity, antibody-dependent cellular cytotoxicity, and apoptosis.
Chimeric anti-CD20 monoclonal antibody that binds CD20 on B cells and depletes CD20-positive cells via complement-dependent cytotoxicity, antibody-dependent cellular cytotoxicity, and induction of apoptosis.
Rituximab binds CD20 on B cells and induces complement-dependent cytotoxicity and Fc-mediated ADCC by NK cells/macrophages; CD20 crosslinking can also trigger apoptosis.
Autologous tumor-infiltrating lymphocyte (TIL) adoptive cell therapy; ex vivo–expanded patient T cells (primarily CD8+/CD4+) recognize melanoma neoantigens via TCRs and mediate direct tumor cytotoxicity.
Autologous, ex vivo–expanded tumor-infiltrating T cells with native TCRs recognize patient-specific melanoma neoantigens/tumor antigens and mediate direct tumor killing via perforin/granzyme cytotoxicity and cytokine release.
Infused TILs recognize the patient-specific peptide–HLA complex via native TCRs and kill the presenting cell through perforin/granzyme-mediated cytotoxicity (and Fas/FasL apoptosis).
Autologous tumor-infiltrating lymphocyte (TIL) adoptive cell therapy; ex vivo–expanded patient T cells (primarily CD8+/CD4+) recognize melanoma neoantigens via TCRs and mediate direct tumor cytotoxicity.
Autologous, ex vivo–expanded tumor-infiltrating T cells with native TCRs recognize patient-specific melanoma neoantigens/tumor antigens and mediate direct tumor killing via perforin/granzyme cytotoxicity and cytokine release.
Infused autologous TILs recognize tumor peptide–HLA via native TCRs and directly kill target cells by immunologic synapse formation with perforin/granzyme release (and Fas–FasL–mediated apoptosis), aided by cytotoxic cytokines.