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).
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.
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).
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.
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.
Autologous, gene-modified CD19-directed chimeric antigen receptor T-cell therapy administered intravenously; engineered patient T cells express an anti-CD19 CAR to recognize and eliminate CD19+ B cells (naive, memory, plasmablasts), inducing B-cell aplasia and reducing autoreactive B cells and pathogenic autoantibodies in SLE.
Autologous T cells are engineered ex vivo to express an anti-CD19 chimeric antigen receptor. After infusion, these CAR-T cells bind CD19 on B-lineage cells (naive, memory, plasmablasts) and kill them via T-cell activation and cytolysis, leading to B-cell aplasia and reduction of autoreactive B cells and pathogenic autoantibodies in SLE.
Anti-CD19 CAR-T cells bind CD19 on B cells, become activated, and induce target-cell death via perforin/granzyme-mediated cytolysis and Fas/FasL apoptosis.
A TROP2-targeted antibody–drug conjugate that binds TROP2 on tumor cells, is internalized, and releases a camptothecin-derived topoisomerase I inhibitor payload to induce DNA damage and cell death (with potential bystander effect).
TROP2-targeted antibody–drug conjugate that binds TROP2 on tumor cells, is internalized, and releases a camptothecin-derived topoisomerase I inhibitor payload to cause DNA damage and tumor cell death, with potential bystander effect.
The ADC binds TROP2 on tumor cells, is internalized, and releases a camptothecin-derived topoisomerase I inhibitor that induces DNA damage leading to apoptosis; the payload can also cause a bystander effect.