An autologous, dual-target CD19/BCMA chimeric antigen receptor T-cell (CAR-T) therapy engineered to deplete CD19+ B cells and BCMA+ plasmablasts/plasma cells to ablate autoreactive B-cell compartments in refractory SLE.
Autologous T cells engineered with dual CARs targeting CD19 and BCMA bind B cells and plasmablasts/plasma cells, triggering CAR signaling that activates T-cell proliferation and cytolytic activity (perforin/granzyme and cytokines) to deplete CD19+ and BCMA+ compartments, thereby abrogating autoreactive B-cell populations and autoantibody production in refractory SLE.
BCMA-targeted CAR-T cells bind BCMA+ cells, activate, and kill them via T-cell cytolysis (perforin/granzyme release and cytokine-mediated apoptosis).
Autologous gene-modified T cells engineered to express a second-generation anti-GD2 chimeric antigen receptor (CD3ζ plus co-stimulatory domain), coexpressing interleukin-15 to enhance persistence and expansion, and incorporating an inducible caspase-9 (iC9) safety switch for controlled elimination.
Autologous T cells genetically engineered to express a second-generation anti-GD2 CAR (CD3zeta plus a co-stimulatory domain) that redirects T-cell recognition and cytotoxicity against GD2-positive tumor cells; coexpressed IL-15 enhances T-cell persistence and expansion in vivo; an inducible caspase-9 (iC9) safety switch enables pharmacologic elimination of the cells to control toxicity.
Anti-GD2 CAR T cells recognize GD2 on target cells and kill them via T-cell cytotoxic mechanisms (perforin/granzyme release and death-receptor pathways).
An anti-HER2 antibody–drug conjugate (RC48) linking a humanized anti‑HER2 monoclonal antibody to the cytotoxic payload monomethyl auristatin E (MMAE). Binds HER2 on urothelial tumor cells, is internalized, and releases MMAE to disrupt microtubules, causing cell-cycle arrest and apoptosis; Fc-mediated effects and a bystander effect may contribute.
Humanized anti-HER2 monoclonal antibody linked via a cleavable linker to monomethyl auristatin E (MMAE). After binding HER2 on tumor cells and internalization, MMAE is released to inhibit tubulin polymerization and disrupt microtubules, leading to G2/M cell-cycle arrest and apoptosis; Fc-mediated effector functions and a bystander effect may also contribute.
The anti-HER2 ADC binds HER2 on tumor cells, is internalized, and releases MMAE, which inhibits tubulin polymerization, disrupting microtubules and causing G2/M arrest and apoptosis (with possible Fc-mediated and bystander contributions).
TROP2-targeting antibody–drug conjugate (izalontamab brengitecan; also referred to as BMS-986507) that delivers a DNA topoisomerase I inhibitor payload to tumor cells, causing DNA damage and cell death with potential bystander effect.
TROP2-targeting antibody–drug conjugate (izalontamab brengitecan; BMS-986507) that binds TROP2 on tumor cells, is internalized, and releases a DNA topoisomerase I inhibitor payload, inducing DNA damage and tumor cell death with a potential bystander effect.
BL-B01D1 is an anti-EGFR/anti-HER3 antibody–drug conjugate that binds EGFR on tumor cells, is internalized, and releases a cytotoxic payload (e.g., topoisomerase I inhibitor), causing DNA damage and tumor cell death, with potential bystander effect.
TROP2-targeting antibody–drug conjugate (izalontamab brengitecan; also referred to as BMS-986507) that delivers a DNA topoisomerase I inhibitor payload to tumor cells, causing DNA damage and cell death with potential bystander effect.
TROP2-targeting antibody–drug conjugate (izalontamab brengitecan; BMS-986507) that binds TROP2 on tumor cells, is internalized, and releases a DNA topoisomerase I inhibitor payload, inducing DNA damage and tumor cell death with a potential bystander effect.
BL-B01D1 is a bispecific ADC that binds HER3 (and EGFR) on tumor cells, is internalized, and releases a cytotoxic payload inside the cell, leading to death of HER3-expressing cells.