Fully human afucosylated IgG1 monoclonal antibody targeting the BAFF receptor (BAFF-R/BR3/TNFRSF13C); blocks BAFF binding to BAFF-R and depletes BAFF-R–expressing B cells via enhanced ADCC/ADCP, reducing autoreactive B-cell activity.
Ianalumab is a fully human afucosylated IgG1 monoclonal antibody that binds the BAFF receptor (BAFF-R/TNFRSF13C), blocks BAFF-BAFF-R signaling, and depletes BAFF-R–expressing B cells via enhanced antibody-dependent cellular cytotoxicity and phagocytosis, reducing survival and activity of autoreactive B cells.
YES
DIRECT
Ianalumab binds BAFF-R on B cells and, via its afucosylated IgG1 Fc, engages Fcγ receptors on effector cells to trigger ADCC and ADCP (NK cell–mediated lysis and macrophage phagocytosis), depleting BAFF-R–expressing cells; BAFF signaling blockade may also promote apoptosis.
First-generation BCR-ABL tyrosine kinase inhibitor used to suppress leukemic proliferation in CML.
ATP-competitive tyrosine kinase inhibitor targeting BCR-ABL (and also PDGFR and KIT), blocking downstream phosphorylation signaling to suppress proliferation and induce apoptosis of malignant cells (e.g., CML; GIST via KIT).
YES
DIRECT
ATP-competitive inhibition of the BCR::ABL1 tyrosine kinase blocks survival/proliferation signaling (e.g., PI3K/AKT, RAS/MAPK, STAT), causing cell-cycle arrest and apoptosis of BCR::ABL1-positive cells.
HER2-targeted antibody–drug conjugate (RC48) that binds HER2 on tumor cells, is internalized, and releases the microtubule inhibitor MMAE to induce cell death (with potential bystander effect).
HER2-directed antibody–drug conjugate that binds HER2 on tumor cells, is internalized, and releases the microtubule inhibitor MMAE to disrupt tubulin polymerization, causing G2/M arrest and apoptotic cell death, with potential bystander effect.
YES
DIRECT
The ADC binds HER2 on target cells, is internalized, and releases MMAE, which disrupts microtubules causing G2/M arrest and apoptotic cell death (with potential bystander effect).
HER2-targeted antibody–drug conjugate (RC48) that binds HER2 on tumor cells, is internalized, and releases the microtubule inhibitor MMAE to induce cell death (with potential bystander effect).
HER2-directed antibody–drug conjugate that binds HER2 on tumor cells, is internalized, and releases the microtubule inhibitor MMAE to disrupt tubulin polymerization, causing G2/M arrest and apoptotic cell death, with potential bystander effect.
NO
INDIRECT
The ADC targets HER2 for uptake; after internalization it releases MMAE, which binds tubulin and disrupts microtubules to cause G2/M arrest and apoptosis. Tubulin expression alone does not make cells targets—killing depends on HER2-mediated delivery (with possible bystander effect).
BCMA-targeting antibody–drug conjugate (humanized anti-BCMA mAb linked to monomethyl auristatin F) that binds BCMA on malignant plasma cells, is internalized, and releases MMAF to disrupt microtubules and induce apoptosis; Fc effector function may contribute ADCC/ADCP.
Afucosylated humanized anti-BCMA monoclonal antibody linked to the microtubule inhibitor MMAF. Binds BCMA on malignant plasma cells and is internalized; intracellular MMAF inhibits tubulin polymerization, causing G2/M arrest and apoptosis. The Fc region can also mediate ADCC/ADCP.
YES
DIRECT
Belantamab mafodotin binds BCMA on target cells, is internalized, and releases MMAF that inhibits tubulin polymerization, causing G2/M arrest and apoptosis; its Fc region can also mediate ADCC/ADCP against BCMA-expressing cells.