A HER2-targeted antibody–drug conjugate linking the anti-HER2 antibody disitamab to the microtubule inhibitor monomethyl auristatin E (MMAE) via a cleavable linker; upon HER2 binding and internalization, MMAE is released to disrupt microtubules, causing G2/M arrest and apoptosis with a potential bystander effect.
HER2-targeted antibody–drug conjugate linking disitamab to the microtubule inhibitor MMAE via a cleavable linker; upon HER2 binding and internalization, the linker is cleaved to release MMAE, which inhibits tubulin polymerization, causing microtubule disruption, G2/M arrest, and apoptosis, with a potential bystander effect.
ADC binds HER2 on target cells, is internalized, and releases MMAE, which inhibits tubulin polymerization causing microtubule disruption, G2/M arrest, and apoptosis (with potential bystander effect).
Autologous T cells genetically modified to express a chimeric antigen receptor targeting CD5; CAR engagement induces MHC-independent T-cell activation, expansion, cytokine release, and perforin/granzyme-mediated cytotoxicity against CD5+ malignant T cells, with potential on-target effects on normal CD5+ T cells.
Autologous T cells are engineered to express a chimeric antigen receptor targeting CD5. CAR engagement on CD5+ cells triggers MHC-independent T-cell activation and expansion, leading to cytokine release and perforin/granzyme-mediated cytotoxicity against CD5-expressing malignant T cells, with potential on-target effects on normal CD5+ T cells.
CAR T cells bind CD5 on target cells, forming an immune synapse and inducing perforin/granzyme-mediated cytolysis (and death receptor pathways), killing CD5+ cells.
Chimeric IgG1 anti-CD20 monoclonal antibody that depletes CD20+ B cells via ADCC/CDC and apoptosis.
Chimeric IgG1 anti-CD20 monoclonal antibody that binds CD20 on B cells and depletes CD20-positive cells via antibody-dependent cellular cytotoxicity (ADCC), complement-dependent cytotoxicity (CDC), and apoptosis.
Anti-CD20 IgG1 binds CD20 on B cells and triggers Fc-mediated ADCC by effector cells, activates complement (CDC), and can induce apoptosis upon crosslinking.
Anti-CD30 IgG1 antibody–drug conjugate (ADC) linked to monomethyl auristatin E (MMAE), a microtubule inhibitor. After binding CD30 and internalization, MMAE is released to disrupt microtubules and induce apoptosis. Used in this trial both unlabeled (predose) and as a radiolabeled PET tracer.
Anti-CD30 IgG1 antibody–drug conjugate linked via a valine–citrulline cleavable linker to monomethyl auristatin E (MMAE). After binding CD30 and internalization into CD30-positive cells, the linker is proteolytically cleaved to release MMAE, which inhibits tubulin polymerization, causing G2/M arrest and apoptosis.
Anti-CD30 ADC binds CD30 on target cells, is internalized, the valine–citrulline linker is cleaved to release MMAE, which inhibits tubulin polymerization causing G2/M arrest and apoptosis.
Anti-HER2 antibody–drug conjugate (RC48) that binds HER2, is internalized, and releases the microtubule inhibitor MMAE to induce cell-cycle arrest/apoptosis; may also mediate ADCC.
An anti-HER2 IgG1 antibody–drug conjugate that binds HER2 on tumor cells, is internalized, and releases the microtubule inhibitor MMAE to block tubulin polymerization, causing G2/M arrest and apoptosis; the antibody component may also mediate ADCC.
The anti-HER2 ADC binds HER2, is internalized, and releases MMAE, which inhibits microtubule polymerization causing G2/M arrest and apoptosis; the IgG1 Fc can also mediate ADCC against HER2+ cells.