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.
NO
INDIRECT
Killing is directed at GD2-positive cells via CAR-mediated T-cell cytotoxicity (perforin/granzyme). The common gamma chain is part of IL-15 receptor signaling on T cells and is not a cytotoxic target.
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.
YES
DIRECT
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).
MicAbody adaptor protein (bispecific antibody; also known as ASP101G) that binds CD20 and carries an orthogonal NKG2D ligand to dock and activate ASP2802 convertible CAR T cells, enabling titratable on/off targeting.
MA-20 (ASP101G) is a MicAbody bispecific adaptor that binds CD20 on B cells and carries an orthogonal NKG2D ligand to engage and activate ASP2802 convertible CAR T cells. By bridging CD20+ tumor cells to the engineered CAR T receptor, it enables titratable, on/off CAR T cytotoxic activity against CD20-positive malignancies.
NO
INDIRECT
The orthogonal NKG2D on ASP2802 CAR T cells serves as a docking receptor. MA-20 bridges CD20 on tumor cells to this receptor, activating CAR T cells to kill CD20+ targets via perforin/granzyme cytolysis; NKG2D-expressing CAR T cells are not killed.
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.
NO
INDIRECT
Cytotoxicity is mediated by the anti-GD2 CAR, which directs T cells to kill GD2-positive cells via perforin/granzyme and death-receptor pathways. IL-15 expression supports T-cell persistence and does not target or kill IL-15Rα-expressing cells.
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.
YES
DIRECT
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.