An anti-HER2 antibody–drug conjugate administered IV every 6 weeks (2.2 mg/kg). The monoclonal antibody targets HER2, is internalized, and releases the auristatin-derived microtubule inhibitor Amberstatin-269 to disrupt tubulin polymerization, causing G2/M arrest and apoptosis; the antibody component may also inhibit HER2 signaling and mediate ADCC.
HER2-targeted monoclonal antibody-drug conjugate. After binding HER2 and internalization, it releases an auristatin (MMAF analog) payload that inhibits microtubule polymerization, causing G2/M arrest and apoptosis; the antibody component may also inhibit HER2 signaling and mediate antibody-dependent cellular cytotoxicity (ADCC).
NO
INDIRECT
ARX788 targets HER2, not CD16a. It kills HER2+ cells via internalization and release of an MMAF payload that inhibits microtubules; its Fc can engage CD16a on NK cells to drive ADCC against HER2+ cells. CD16a+ cells are effectors, not targets.
Autologous CAR-T cells incorporating an NKG2D-based receptor to bind stress-induced ligands (e.g., MICA, MICB, ULBPs) on tumor cells, triggering T-cell activation and cytotoxicity across diverse tumors.
Autologous T cells engineered to express an NKG2D-based chimeric antigen receptor that binds stress-induced ligands (e.g., MICA, MICB, ULBPs) on tumor cells, initiating CD3ζ/costimulatory signaling to activate T cells, drive cytokine release and proliferation, and mediate MHC-independent cytotoxic tumor killing.
YES
DIRECT
CAR-T cells bind ULBP4 (an NKG2D ligand) on target cells, triggering CD3ζ/costimulatory signaling and T-cell cytotoxicity via perforin/granzyme (and death receptor) pathways, causing MHC-independent lysis/apoptosis.
Autologous CAR-T cells incorporating an NKG2D-based receptor to bind stress-induced ligands (e.g., MICA, MICB, ULBPs) on tumor cells, triggering T-cell activation and cytotoxicity across diverse tumors.
Autologous T cells engineered to express an NKG2D-based chimeric antigen receptor that binds stress-induced ligands (e.g., MICA, MICB, ULBPs) on tumor cells, initiating CD3ζ/costimulatory signaling to activate T cells, drive cytokine release and proliferation, and mediate MHC-independent cytotoxic tumor killing.
YES
DIRECT
NKG2D-based CAR T cells bind ULBP5 on target cells, activating CD3zeta/costimulatory signaling and inducing perforin/granzyme-mediated lysis (and Fas–FasL apoptosis) of the bound cells.
Autologous CAR-T cells incorporating an NKG2D-based receptor to bind stress-induced ligands (e.g., MICA, MICB, ULBPs) on tumor cells, triggering T-cell activation and cytotoxicity across diverse tumors.
Autologous T cells engineered to express an NKG2D-based chimeric antigen receptor that binds stress-induced ligands (e.g., MICA, MICB, ULBPs) on tumor cells, initiating CD3ζ/costimulatory signaling to activate T cells, drive cytokine release and proliferation, and mediate MHC-independent cytotoxic tumor killing.
YES
DIRECT
NKG2D-based CAR-T cells bind ULBP6 on target cells, activate via CD3ζ/costimulatory signaling, form an immune synapse, and kill the bound cells through perforin/granzyme (and death-receptor) pathways.
Anti-HER2 antibody–drug conjugate (trastuzumab deruxtecan/Enhertu) that targets HER2, internalizes, and releases a deruxtecan topoisomerase I inhibitor payload to induce DNA damage in tumor cells.
HER2-targeted antibody–drug conjugate composed of trastuzumab linked to deruxtecan (a topoisomerase I inhibitor). After HER2 binding and internalization, the payload is released to inhibit Top1, causing DNA damage, cell cycle arrest, and apoptosis; also elicits ADCC and a bystander killing effect.
YES
DIRECT
Binds HER2, is internalized, and releases a deruxtecan Top1 inhibitor payload causing DNA damage and apoptosis; also induces ADCC and bystander killing.