Polyclonal antibody preparation that depletes T cells to reduce graft rejection and GVHD.
Polyclonal anti–T-cell immunoglobulins that bind multiple T-cell surface antigens and deplete T cells via complement-dependent cytotoxicity, antibody-dependent cellular cytotoxicity, and phagocytic clearance, producing immunosuppression to prevent graft rejection and GVHD.
NO
INDIRECT
ATG is a polyclonal anti‑T‑cell antibody mixture that binds T‑cell antigens (e.g., CD2, CD3, CD4, CD8) and depletes T cells via complement activation, ADCC, and phagocytic clearance; it does not specifically target HLA‑DR, so HLA‑DR–expressing cells are not directly killed.
An antibody–drug conjugate (RC48) composed of a humanized anti-HER2 IgG linked via a cleavable linker to the cytotoxic payload MMAE. It binds HER2 (including low-expressing tumors), is internalized, and releases MMAE to inhibit tubulin polymerization, inducing mitotic arrest and apoptosis with potential bystander killing.
Humanized anti-HER2 IgG (disitamab) linked via a cleavable linker to the microtubule-disrupting payload MMAE. After binding HER2 (including low-expressing tumors) and internalization, intracellular cleavage releases MMAE, which inhibits tubulin polymerization, leading to G2/M cell-cycle arrest, apoptosis, and potential bystander killing.
YES
DIRECT
Anti-HER2 ADC binds HER2, is internalized, and releases MMAE that disrupts microtubules, causing G2/M arrest and apoptosis (with possible bystander killing).
An antibody–drug conjugate (RC48) composed of a humanized anti-HER2 IgG linked via a cleavable linker to the cytotoxic payload MMAE. It binds HER2 (including low-expressing tumors), is internalized, and releases MMAE to inhibit tubulin polymerization, inducing mitotic arrest and apoptosis with potential bystander killing.
Humanized anti-HER2 IgG (disitamab) linked via a cleavable linker to the microtubule-disrupting payload MMAE. After binding HER2 (including low-expressing tumors) and internalization, intracellular cleavage releases MMAE, which inhibits tubulin polymerization, leading to G2/M cell-cycle arrest, apoptosis, and potential bystander killing.
NO
INDIRECT
The ADC binds HER2 on tumor cells, is internalized, and releases MMAE, which then binds β‑tubulin to disrupt microtubules causing G2/M arrest and apoptosis (with possible bystander killing). Tubulin is the payload’s intracellular target, not the antigen used for cell targeting.
Oral small-molecule BCL-2 inhibitor that blocks anti-apoptotic BCL-2 to restore mitochondrial (intrinsic) apoptosis in malignant B cells.
Oral small-molecule BCL-2 inhibitor that blocks the anti-apoptotic BCL-2 protein, promoting BAX/BAK activation and restoring mitochondrial (intrinsic) apoptosis in malignant B cells.
YES
DIRECT
Inhibits anti‑apoptotic BCL‑2 in target cells, freeing pro‑apoptotic factors to activate BAX/BAK, causing mitochondrial outer membrane permeabilization, cytochrome c release, caspase activation, and intrinsic apoptosis.
Type II, glycoengineered anti-CD20 monoclonal antibody that depletes CD20+ B cells via enhanced ADCC and direct cell death.
Type II, glycoengineered anti-CD20 IgG1 monoclonal antibody that binds CD20 on B cells and, via enhanced FcγRIIIa engagement (afucosylated Fc), drives potent antibody-dependent cellular cytotoxicity (ADCC) and direct, caspase-independent cell death, leading to depletion of CD20+ B cells.
YES
DIRECT
Obinutuzumab binds CD20 on B cells and recruits effector cells via enhanced Fc gamma RIIIa engagement to mediate ADCC/ADCP, and also induces direct, caspase-independent cell death of CD20+ cells.